Therapeutic role of essential oils in atopic dermatitis: A review

Jiawei Duan; Fei Luan; Jinkai li; Junbo Zou; Jing Sun; Yajun Shi; Dongyan Guo; Yundong Xie; Huanxian Shi; Changli Wang; Xiao Wang; Xiaofei Zhang

doi:10.25259/AJC_11_2024

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Review Article

2025

:18;

112024

doi:

10.25259/AJC_11_2024

Therapeutic role of essential oils in atopic dermatitis: A review

Jiawei Duan, Fei Luan, Jinkai li, Junbo Zou, Jing Sun, Yajun Shi, Dongyan Guo, Yundong Xie, Huanxian Shi, Changli Wang, Xiao Wang, Xiaofei Zhang^,*

Key Laboratory of Basic and New Drug Research in Chinese Medicine, Shaanxi University of Chinese Medicine, Xianyang, 712046, Shaanxi, China

*Corresponding author: E-mail address: 2051028@sntcm.edu.cn (X. Zhang)

Received: 2024-09-10, Accepted: 2025-05-31, Epub ahead of print: 2025-08-20, Published: 2025-08-23

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This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

Abstract

Atopic dermatitis (AD) is a prevalent inflammatory skin disorder. Its pathogenesis is influenced by multiple factors that impair both physical and psychological well-being. Traditional treatments, including corticosteroids, calcium-modulated phosphatase inhibitors, antibiotics, and other agents, are often linked to significant side effects, the risk of drug resistance, and the potential for secondary harm. In contrast, essential oils derived from natural plants have shown promising therapeutic effects against AD. These oils exhibit biological activities such as anti-inflammatory, antimicrobial, and antioxidant effects while maintaining low toxicity and minimal side effects. Such properties enable essential oils to modulate immune responses, enhance skin barrier function, and regulate microbial ecosystems, thereby exerting favorable anti-inflammatory and antibacterial effects. This review explores the pathogenesis of AD and the mechanisms through which essential oils contribute to its management, highlighting key natural essential oils and their active components with therapeutic potential for AD. Additionally, it contrasts the benefits and drawbacks of conventional therapies versus essential oils in AD treatment. The review also discusses notable examples of essential oil applications in clinical AD trials, aiming to support the development of novel therapeutic strategies for dermatitis and lay the groundwork for future research in AD treatment.

Keywords

Atopic dermatitis

Essential oil

Mechanism

Monomer

Pathogenesis

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1. Introduction

Atopic dermatitis (AD) is an inflammatory skin condition affecting the dermis and superficial epidermis, resulting from the interplay of various factors. Its etiology is multifaceted, typically classified into intrinsic and extrinsic causes. Intrinsic factors include allergies, immune imbalances, epidermal dysfunction, and genetic predispositions [1,2], while extrinsic factors encompass increased air pollution and dietary changes. Studies indicate that AD predominantly affects children, with a prevalence of approximately 20% in developed countries and an increasing incidence in developing regions [3], Although not life-threatening, AD can significantly impact physical and psychological well-being. The disease, whether acute or chronic, begins with symptoms such as erythema, papules, and blisters, progressing to epidermal ulcers, which can severely affect the skin. Research underscores a strong correlation between AD and mental health issues, including depression, anxiety, and suicidal ideation [4], highlighting the urgency of timely intervention.

AD presents a prolonged course and significant therapeutic challenges [5]. Therefore, the main principles of treatment, as directed by national and international guidelines (Appendix), are employing emollients to restore the skin’s surface barrier, alongside the utilization of topical anti-inflammatory therapies, such as corticosteroids or analogs of calcium-modulated phosphatase inhibitors. Conversely, in severe cases, effective and standardized interventions are required, such as phototherapy or immunosuppressive agents, to alleviate symptoms and reduce recurrence [4]. However, conventional therapies have several limitations. While corticosteroids offer symptom relief, they are associated with substantial adverse effects. Excessive reliance on topical calcium-modulated phosphatase inhibitors can lead to transient burning sensations at the application site, potentially exacerbating the condition and contributing to recurrent or prolonged episodes of AD. These drawbacks underscore the critical need for the development of safe, effective, and reliable natural treatments.

Essential oils, also known as volatile oils, are natural secondary metabolites found in the epidermal glandular hairs, oil chambers, oil cells, and oil ducts of aromatic plants [6]. Since ancient Egypt, essential oils derived from aromatic plants have been utilized in massage therapy and aromatherapy for disease prevention and treatment. These oils are widely recognized for their antibacterial, anti-inflammatory, anticancer, and antioxidant properties [7]. Such properties influence skin tissues by regulating the local microecological environment and altering the biofactors and physiological structure of the skin, thus promoting wound healing and enhancing skin barrier repair [8]. Research has demonstrated the therapeutic potential of essential oils for skin disorders. For example, tea tree oil alleviates symptoms of skin irritation, while geranium essential oil reduces skin inflammation [9]. Additionally, essential fatty acids (EFAs) have shown beneficial effects on atopic diseases. Clinical trials indicate that evening primrose oil (EPO) increases plasma EFA concentrations, significantly alleviating dermatitis symptoms [10]. Furthermore, blackcurrant seed oil, rich in EFAs, helps correct EFA imbalances and temporarily reduces the prevalence of AD [11].

Essential oils exhibit promising effects and research potential in AD treatment. This review explores the pathogenesis of AD, examines the mechanisms through which essential oils contribute to AD management, and discusses the therapeutic potential of essential oil monomers, providing valuable insights for the development of novel drugs for AD treatment in future research.

2. Pathogenesis of AD

AD is a prevalent dermatological disorder characterized by polymorphic lesions, including erythema, papules, blisters, vesicles, and scabs. It is frequently accompanied by intense itching and inflammatory skin infections, significantly impairing both physical and mental well-being, thus impacting daily functioning [12]. The pathogenesis of AD is multifactorial, involving genetic and environmental factors, immune dysfunction, microbial imbalance, and skin barrier dysfunction [13].

2.1. Genetic and environmental factors

Genetic factors account for 82% of the risk for developing AD, while environmental factors contribute 18% [14]. The genetic basis of AD is largely attributed to specific familial histories and functional mutations in the filaggrin (FLG) gene, a key protein involved in filament polymerization [15]. FLG, present in the epidermal granule cell layer, plays a critical role in maintaining the skin’s stratum corneum (SC) barrier function and facilitating the movement of intracellular metabolites [16]. Mutations in the FLG2 gene have been linked to persistent AD [17]. Recent studies suggest that FLG deficiency leads to skin barrier disruption, enabling allergens to penetrate the epidermis, thereby triggering inflammatory vesicle formation, protease activation, and microbial colonization [18]. In addition to FLG, other genes, such as loricrin (LOR), are associated with AD. LOR, a major component of the keratinized envelope, is more prevalent in European populations, while FLG mutations are more common in Asian populations. A family history of atopic diseases, including asthma, allergic rhinitis, and food allergies, increases the likelihood of AD development. Epidemiological studies show that if one parent has an atopic disease, the risk of the child developing an atopic condition exceeds 50%, which rises to 80% if both parents are affected [19]. Children with severe AD are also prone to food allergies, and more than 50% may develop asthma [20]. Environmental factors also play a significant role in AD pathogenesis. High humidity, prolonged periods of inadequate cleaning leading to damp conditions, and an increase in mildew, bacteria, and microbial growth, as well as exposure to dietary allergens, can all exacerbate AD symptoms.

2.2. Skin barrier dysfunction

The skin barrier is a critical protective structure, consisting of the SC on the skin surface and the lipids between keratinocytes [21]. The SC is essential for maintaining skin barrier function, preventing water loss, shielding against environmental pollutants, and protecting against microbial and pathogenic invasion. The integrity of the skin barrier relies heavily on intercellular lipids, and deficiencies in these lipids can result in barrier dysfunction. Trans-epidermal water loss (TEWL) is commonly used to assess barrier function in individuals with AD, serving as a reliable and objective measure. In AD, the skin barrier is compromised, leading to reduced hydration of the SC, increased TEWL, and a failure of FLG in keratinocytes to properly bind to keratin fibers in the SC, undermining barrier integrity. Both dry skin and irregular TEWL are linked to silk protein deficiency in patients with AD. Moreover, TEWL inversely correlates with the mRNA expression of FLG and LOR, as demonstrated in skin biopsies [22]. Early-onset AD resulting from FLG deficiency increases susceptibility to skin irritation and infection. Elevated serum immunoglobulin E (IgE) levels, coupled with increased skin permeability to irritants and pathogens, foster microbial growth that further damages the skin. This weakened skin barrier is particularly vulnerable to colonization by Staphylococcus aureus (S. aureus), which contributes to cutaneous inflammation. The ensuing inflammatory response disrupts epidermal differentiation, ultimately impairing the skin barrier’s function [23].

2.3. Microbial ecological imbalance

Microbial ecological imbalance plays a pivotal role in the pathogenesis of AD. The severity of AD is closely associated with reduced microbiome diversity and increased colonization by pathogenic bacteria, particularly S. aureus [24] Investigations have shown that S. aureus has a significant pathogenic relationship with AD. The colonization rate of S. aureus in AD lesions can range from 30% to 100%, compared to just 20% in healthy skin [25]. The microbial ecological balance is determined by the competition among species. On the skin of individuals with AD, a competitive interaction exists between S. aureus and other bacterial populations. The overall bacterial diversity in normal skin is greater, and the microbial community is more stable. In AD, the skin barrier is compromised, and S. aureus undergoes adaptive evolution driven by competition within the AD skin microenvironment, resulting in a reduction of its competitive interactions on the skin [26]. S. aureus colonizes in large numbers on the skin, leading to a reduction in microbial diversity. This disruption in microbial balance contributes to an ecological imbalance in the skin microbiome, ultimately exacerbating the severity of AD. S. aureus is one of the primary bacterial pathogens responsible for both superficial and invasive skin infections, contributing significantly to the global burden of skin infections [27]. As early as 1970, it was recognized that individuals with AD exhibit a compromised skin barrier, characterized by increased S. aureus colonization, which exacerbates skin barrier dysfunction and inflammation [28]. S. aureus induces inflammation through mechanisms such as T cell-independent B-cell expansion and the production of pro-inflammatory cytokines [29]. Studies have shown that 90% of patients with AD carry S. aureus. This bacterium has evolved sophisticated mechanisms to produce a wide array of cell wall proteins and utilizes both physical and chemical strategies to adhere to the skin, disrupting the skin barrier. Furthermore, S. aureus membrane vesicles (MVs) have been implicated in worsening AD by efficiently delivering bacterial effector molecules into host cells, playing a key role in the progression of the condition [30].

2.4. Immune dysfunction

AD is an allergic and inflammatory skin disorder with a multifactorial etiology. Immune dysfunction is a key pathogenic mechanism in AD. A primary immune response contributing to the condition is the imbalance in the differentiation of T helper cell 1 (Th1) and T helper cell 2 (Th2). Dysregulation in the differentiation of T helper cell 17 (Th17) and regulatory T-cells (Tregs) also plays a critical role in AD pathogenesis. CD4⁺ T-cells, which are essential to the human immune system, can differentiate into Th1 and Th2 cells. Maintaining immune homeostasis between Th1 and Th2 is vital for the development and progression of various immune-related diseases. This balance is predominantly governed by Th1 cells, with the participation of Th2 cells, which primarily secrete cytokines such as interleukin (IL)-4, IL-25, and IL-5. In contrast, Th1 cells mainly produce IL-2, tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) [31]. In AD, an imbalance in Th1/Th2 differentiation leads to increased IL-4 and IL-5 secretion by Th2 cells, which exacerbates the condition. Elevated IL-4 levels inhibit Th1 cells, reducing the production of IL-2 and IFN-γ, while simultaneously promoting Th2 cell proliferation, stimulating B cells to produce excessive IgE and eosinophils, thereby triggering allergic responses and worsening inflammation [32]. In addition, Th17 cells are primarily involved in AD pathogenesis. These cells secrete IL-23, IL-17, and IL-6, co-induced by IL-6 and transforming growth factor-β (TGF-β). Tregs play a pivotal role in maintaining immune tolerance, inactivating effector T-cells, and regulating immune responses by producing cytokines such as TGF-β and IL-10. However, in AD, the role of Th17 cells and their cytokines becomes predominant, promoting inflammation, while Tregs assume an immunosuppressive role and exhibit a marked decrease in the Th17/Treg cell ratio [33]. Th17 cells and Tregs exhibit antagonistic behavior. In AD, the imbalance in Th17/Treg differentiation, along with the excessive production of IL-6, inhibits Treg expression, thereby favoring Th17 cell differentiation. With the involvement of IL-23, activated Th17 cells transition into pathogenic Th17 cells, which secrete substantial amounts of IL-17. This promotes neutrophil aggregation and cellular infiltration, further intensifying inflammation at the site of infection [34]. An illustrative depiction of this mechanism has been presented in Figure 1.

Schematic diagram of the pathogenesis of AD caused by the aforementioned factors.

3. Advancements in essential oil research for AD treatment

3.1. Inhibition of S. aureus colonization by essential oils

Essential oils are renowned for their antibacterial properties and have been widely used to treat various skin disorders. Pathogenic microorganisms, particularly S. aureus, significantly impact the severity of AD lesions by inducing oxidative skin damage and inflammation. Studies show that up to 90% of patients with AD harbor S. aureus [35], with a single lineage of S. aureus typically dominating the population in these patients [36]. Cellular model studies have demonstrated that essential oils can provide protective benefits against S. aureus-induced skin damage [37]. By inhibiting the proliferation of S. aureus, essential oils reduce pathogenic bacterial colonization, enhance microbiome diversity, and promote therapeutic effects in dermatitis [14]. Kwon et al. [35] reported that disrupting S. aureus MVs reduced Th1, Th2, and Th17 cell-mediated inflammatory responses, leading to decreased expression of inflammatory cytokines such as IL-1β, IL-6, TNF-α, and chemokines. Thymol, a compound found in thyme essential oil, has been shown to attenuate cytotoxicity and inflammatory responses by targeting S. aureus MVs. Thus, topical application of thymol may mitigate AD exacerbation triggered by S. aureus MVs. Furthermore, Zhang et al. [37] demonstrated that grapefruit essential oil promotes the proliferation of human immortalized keratinocytes (HaCaT cells), reduces reactive oxygen species (ROS) production induced by S. aureus metabolites, and inhibits the overexpression of IL-1 and cyclooxygenase-2 (COX-2), thus alleviating the inflammatory response. These effects were evident in studies analyzing the anti-inflammatory and antioxidant properties of grapefruit essential oil, which also contributed to epidermal cell repair and protection against S. aureus metabolite-induced damage [38]. These findings suggest that grapefruit essential oil exhibits both anti-inflammatory and antioxidant properties, along with skin-repairing effects. Thus, essential oils can inhibit S. aureus colonization on the skin by disrupting S. aureus MVs and reducing the harmful effects of S. aureus metabolites. An illustrative depiction of this mechanism has been presented in Figure 2.

Schematic diagram of the mechanism of action of essential oils in the treatment of AD by inhibiting the colonization of S. aureus.

3.2. Essential oils reduce inflammation by modulating relevant inflammatory factors and pathways

Mast cells, playing a key role in immune responses, secrete various cytokines and inflammatory mediators, playing a pivotal role in the pathogenesis of AD [39]. Essential oils can mitigate AD-related pathological effects stemming from skin barrier dysfunction and immune dysregulation by inhibiting the release of β-hexosaminidase, histamine, and other inflammatory mediators and cytokines from mast cells [40]. Th1 and Th2 cells, both subsets of CD4⁺ T-cells, primarily secrete distinct cytokines—IL-12 and IFN-γ in Th1, and IL-4, IL-5, and IL-13 in Th2—which regulate inflammation by modulating related inflammatory factors, thereby alleviating AD symptoms. Kim et al. [40] elucidated the mechanism of chrysanthemum essential oil (CBFEO) in both in vitro and in vivo models. In vitro experiments using TNF-α-treated HaCaT cells and IgE-sensitized mast cells, along with in vivo studies using 2, 4-dinitrochlorobenzene (DNCB)-induced mouse dermatitis, demonstrated that CBFEO reduced epidermal thickness, inhibited mast cell infiltration, diminished histamine and β-hexosaminidase release, and increased FLG and LOR expression. These effects collectively contributed to reduced inflammation and alleviation of AD-related lesions. Aslam et al. [41] explored the immunomodulatory effects of thymoquinone (TQ) from Nigella sativa essential oil in a mouse model of AD, comparing its efficacy to tacrolimus, a commonly used drug. TQ treatment reduced inflammatory cell counts in the bloodstream, improved macroscopic skin alterations, lowered serum IgE levels, and downregulated IL-4, IL-5, and IFN-γ mRNA expression. Natural plant essential oils can effectively mitigate inflammation by inhibiting cellular inflammatory factors and suppressing mast cell-mediated mediator release, thereby offering therapeutic benefits. Table 1 lists essential oils commonly used for treating skin inflammation.

Table 1. Therapeutic AD anti-inflammatory mechanisms of natural plant essential oils (Increase, ↑; Decrease, ↓).

No	Essential oil	Essential oil active ingredient			Mode of action	Types	Dose/ concentration	Experimental model	Effects/Mechanisms	References
1	Perilla frutescens volatile oil	Limonene	Perilla ketone	Perilla aldehyde	Gavage	In vivo	0.4 mL/kg	Inflammatory model of carrageenan in rats	PGE2 levels ↓; NO levels in inflamed tissues ↓;	[42]
2	Lavandula angustifolia Mill essential oil	Linalool	Linalyl acetate		-	In vitro	0.32 ,0.64 µL/mL	LPS-stimulated mouse macrophage model	The NF-κB pathway↓; iNOS protein levels ↓; NO production ↓;	[43]
3	Houpoea officinalis volatile oil	β-eudesmol,	2-naphthalene methanol		Gavage	In vivo	20,40,60 mg/kg; Once a day; successive one month	A model of foot-plantar swelling induced by carrageenan gum in mice	Inflammatory tissue PGE2↓; TNF-α levels↓; IL-1β levels;	[44]
4	Pelargonium roseum essential oil	Citronellol	Geraniol	Citronellyl formate	Gavage	In vivo	100 mL/kg;	A model of plantar-plantar swelling induced by carrageenan gum	Carrageenan gum-induced foot and claw oedema↓; Inflammatory response of the skin↓;	[45]
5	Curcuma longa L. essential oil	Aromatic turmeric ketone	Curcuminoids		Intraperitoneal injection	In vivo	1 000 mg/kg; Once a day; Successive 5 days;	A model of dextran-induced acute inflammation	Histamine release↓; 5-hydroxytryptamine release↓; prostaglandins release↓; bradykinin release↓;	[46]
6	Citrus medica L. essential oil	Limonene	Linalool	Linalyl acetate	Intraperitoneal injection	In vivo	86.2 mg/kg	A model of foot oedema caused by carrageenan gum	IL-1β levels↓; IL-6 levels↓; TNF-α levels↓; nitrite/nitrate↓; prostaglandin E↓;	[47]
7	Origanum vulgare essential oil	Caryophyllene oxide	β-caryophyllene		Intraperitoneal injection	In vivo	3.5 mg/pc; Experiment lasts 60/75 minutes	formalin test	Mechanisms are unclear	[48]
8	Cymbopogon citratus (D. C.) Stapf essential oil	Citral	Geraniol	Limonene	Ear smear administration	In vivo	0.1, 0.3, and 1.0%	TPA-induced acute dermatitis model	pro-inflammatory cytokines TNF-α and IL-6↓; healing effect↑;	[49]
9	Turmeric Waste Leaf essential Oil	Terpinolene	α-phellandrene		Ear smear administration	In vivo	0.1, 0.3, and 1.0%	TPA-induced acute dermatitis model	Ear weight and thickness↓; protein levels of TNF-α, IL-6 and IL-1β↓; ear oedema↓;	[50]
10	Ginger essential Oil	α-gingerene	β-bisabolene	α-bergamotene	Skin smear administration	In vivo	150 μL/pc	UVB-induced skin inflammation	IL-1β expression in skin tissues↓; TNF-α expression in skin tissues↓;	[51]
11	Angelica sinensis (Oliv.) Diels essential Oil	β-pinene	α-pinene		-	In vitro	40 μg/kg	LPS-stimulated mouse macrophage model	Pro-inflammatory cytokines TNF-α↓; IL-1β↓; IL-6↓; inflammatory mediators HIS↓; 5-HT↓; PGE2↓; NO↓; inflammation-related enzymes iNOS and COX-2↓;	[52,53]
12	Citrus Peel essential Oil	Limonene			Ear smear administration	In vivo	0.1% and 1%	TPA-induced ear inflammation in mice	TPA-induced ear inflammation↓; cytokine levels TNF-α↓; IL-6↓; IL-1β↓;	[54]
13	Zanthoxylum bungeanum Maxim. volatile oil	Linalool	β-pinene	β-caryophyllene	Skin smear administration	In vivo	20 μL/pc; Twice a day; Successive 10 days;	DNCB-induced AD model	Ear swelling↓; skin damage↓; NF-κB activity↓; phosphorylation of MAPKs↓;	[55]
14	Medlar Nematode (Asteraceae) essential Oil	Limonene	Bicyclocerene		Ear smear administration	In vivo	0.1, 0.3 and 1.0 mg/ear; Twice a day; Successive 9 days;	TPA-induced ear inflammation in mice	TPA-induced inflammation in the skin↓; interfering with oedema↓; leukocyte migration↓;	[19]
15	Artemisia carvifolia essential Oil	Eucalyptol	Camphor		Ear smear administration	In vivo	750, 250, 83 mg /kg	TPA-induced ear oedema in mice;	TPA-induced mouse ear oedema↓; COX-2 protein levels↓;	[56]
16	Rosmarinus officinalis essential Oil	Limonene	1,8-cineole		Gavage	In vivo	100 mg / kg	Carrageenan gum-induced paw oedema test in rats	The mechanism is unclear.	[57]
17	Nigella damascena L. essential Oil	Thymoquinone	Thymol		Skin smear administration	In vivo	5 mg/kg; Once a day; Successive 10 days;	Imiquimod (IMQ)-induced psoriasis model	IMQ-induced psoriasis-like inflammation↓; All epidermal and dermal changes↑;	[58]
18	Mentha arvensis Essential Oil	Menthol	Menthone		Skin smear administration	In vivo	1%; Once a day; Successive 14 days;	DNCB-induced AD in BALB/C mice	NLRP3↓; caspase-1↓; NLRP3 inflammatory vesicles↓; IL-1β production ↓;	[59]
19	Nigella damascena L. essential Oil	Plamitic acid	Palmitoleic acid		Skin smear administration	In vivo	200 μL/pc; Once a day; Successive 43 days;	DNCB-induced AD model	The Th2 chemokines TARC and MDC in inflamed skin ↓;	[60]
20	Hedychium flavum flower essential oil	β-pinene	α-pinene	1,8-cineole	Ear smear administration	In vivo	1, 2, and 4 g/kg	Xylene-induced ear oedema in mice	Xylene-induced mouse ear oedema↑; levels of TNF-α↓; IL-6↓; IL-1β↓;	[61]
21	East Indian Sandalwood Oil	α-santalol	β-santalol		Skin smear administration	In vivo	0.001- 0.002 %	Human Full-Thickness Skin Model	psoriasis symptoms↑; pathology↑; inflammatory factors↓;	[62]
22	Artemisia annua L. essential oil	Caryophyllene	Eucalyptol	α-pinene	Skin smear administration	In vivo	3%, 5%, and 10%	DNCB-induced AD model	MAPK/NF-κB signaling pathway↓; TNF-α↓; IL-1β↓; IL-6↓;	[63,64]
23	Baccharis dracunculifolia (Asteraceae) essential oil	β-Caryophyllene	Bicyclogermacrene	Nerolidol	Ear smear administration	In vivo	0.1, 0.3, and 1.0 mg/ear	TPA-induced ear oedema in mice;	oedema formation↓; cellular influx into inflamed tissues↓; keratinisation↓;	[65]
24	Sacha inchi oil	Oleic acid	Linoleic acid,		Skin smear administration	In vivo	100 μL/pc; Once a day; Successive 49 days;	DNFB-induced AD model	p-P38↓; p- ERK↓; p-NF-κB↓; IκBα signaling pathways↓;	[66]

Nuclear factor-κB (NF-κB), a critical transcription factor, is central to regulating the inflammatory response and is modulated by mitogen-activated protein kinases (MAPKs), facilitating the transcription of target genes within the nucleus [67]. NF-κB promotes the secretion of pro-inflammatory cytokines such as IL-6, IL-1β, and TNF-α, while also activating cytokines and chemokines through the MAPK/NF-κB signaling pathway [68]. These molecules are essential for immune cell activation and maintaining skin barrier integrity. Wang et al. [69] employed a novel network pharmacology approach, incorporating the “quantity-efficacy” weighting coefficient method, to show that German chamomile essential oil regulates T-cell subpopulations and inhibits the Th17 cell differentiation pathway. This downregulation of IL-17 suppresses NF-κB and MAPK pathway activation, reducing the secretion of pro-inflammatory cytokines like TNF-α and IL-6, thereby mitigating inflammation. In a separate in vitro study, Kim et al. [70] demonstrated that peppermint volatile oil reduces the phosphorylation of extracellular regulated protein kinases (ERK), a MAPK family member, thereby inhibiting the activation of NF-κB and modulating cellular responses and inflammation-related gene expression. This inhibition of the ERK/NF-κB pathway effectively reduces inflammatory factors, offering therapeutic potential in AD treatment. Li et al. [71] further validated the mechanism of rosemary essential oil in AD therapy through the integration of network pharmacology and metabolomics, demonstrating its role in modulating the Janus kinase (JAK)/Signal transducer and activator of transcription (STAT)/NF-κB pathway and inhibiting arachidonic acid metabolite production to alleviate AD-associated inflammation. These findings underscore the importance of inflammatory pathways, particularly the NF-κB pathway, in AD treatment, with regulation of these pathways leading to decreased inflammatory factors and therapeutic effects. Table 2 outlines the pathways relevant to AD treatment, and Figure 3 provides a visual representation of this mechanism.

Table 2. Therapeutic AD pathway mechanisms of natural plant essential oils. (Increase, ↑; Decrease, ↓).

No	Signaling pathway	Types	Dose/concentration	Animal model	Effects/Mechanisms	References
1	JAK2/STAT5 signaling pathway	In vivo	50 μL/pc; Once a day; Successive 21 days;	DNCB-induced AD mouse model	TNF-α/IFN-γ-induced inflammatory chemokine expression↓; JAK2/STAT5 signaling pathway↑; TNF-α/IFN-γ-induced ROS levels↓;	[72]
2	mTOR/NF-κB signaling pathway essential oil	In vivo	20 μL/pc; Once a day; Successive 29 days;	DNCB-induced AD mouse model	mTOR/NF-κB signaling axis inflammatory response↓;	[73]
3	STAT/MAPK signaling pathways	In vivo	100 μL/pc; Once a day; Successive 29 days;	DNCB-induced AD mouse model	AD-like symptoms↑; Inflammation induced by TNF-α↓; IFN-γ↓;	[74]
4	The MAPKs/NF-kB signaling pathway	In vivo	20 mL/kg, Once a day; Successive 21 days;	DNCB-induced AD mouse model	NLRP3 inflammatory vesicles ↓; activation of the MAPKs/NF-κB signaling pathway↑;	[75]
5	NF-κB/JAK/STAT signaling pathway	In vivo	40 μL/pc; Once a day; Successive 43 days;	DNCB-induced AD mouse model	IFN-γ↓; TNF-α↓; Th2 chemokines TARC↓; Th2 chemokines MDC↓;	[60]
6	Nrf2/HO-1/NF-κB Signaling Pathway	In vitro	1 × 10⁵ cells/mL	LPS-stimulated RAW 264.7 macrophages	Protein expression of inducible nitric oxide synthase (iNOS) ↓; COX-2 ↓;	[76]
7	AGE-RAGE signaling pathway	In vivo	0.18 g/pc; Once a day; Successive 14 days;	Sodium dodecyl sulphate, induction of eczema-like skin lesions	FLG expression↑; the AGE-RAGE signaling pathway↓; inflammation↓; eczema↑;	[77]
8	NF-κB/ERK signaling pathway	In vitro	10 ng/mL	Induction of inflammatory response in HMEC-1 cells	TNF-α-induced nuclear translocation of NF-κB↓; ERK1/2 phosphorylation levels↓;	[78]
9	The MAP2K2/ERK pathway	In vivo	10 mg/kg⁻¹; 20 mg/kg⁻¹; 40 mg/kg⁻¹; Once a day; Successive 15 days;	Squaric acid dibutyl ester-induced mouse model	Acts on JAK-STAT3; MAPK2 activity↓; ERK phosphorylation↓; skin inflammation↓;	[79]
10	PI3K/Akt/mTOR and p38MAPK Signaling Pathway	In vivo	200 μL/time/mice; Twice a day; Successive 7 days;	IMQ-induced psoriasis model	PI3K/Akt/mTOR and p38MAPK pathways↓; IL-22/TNF-α/LPS↓; inflammatory cytokines↓;	[80]

AGE: advanced glycation end products, RAGE: Receptor for advanced glycation end products, PI3K: Phosphatidylinositol-3-kinase

Schematic representation of the mechanism of action of essential oils in the treatment of AD through modulation of inflammatory factors and related pathways.

3.3. Essential oils complement EFAs in alleviating AD

EFA supplementation may alleviate AD [81]. Essential oils are rich in volatile compounds as well as EFAs, which serve as components of cell membranes and precursors to immunomodulatory factors potentially involved in the inflammatory and immunopathogenic processes underlying AD. Early studies have shown that in an EFA-deficient state, the skin manifests symptoms such as erythema, papules, and blisters with inflammatory lesions reminiscent of AD-like skin changes, accompanied by a significant decrease in skin moisture and impaired barrier function [82]. Increased rate of epidermal cell proliferation, increased metabolic activity, sterol ester and abnormal keratin-forming cell formation, and increased colonization by S. aureus [83]. Linoleic acid (LA), a class of EFAs, can be enzymatically converted into gamma-linolenic acid (GLA), an omega-6 EFA. Subsequently, GLA undergoes further metabolism to become dihomo-GLA (DGLA). Impaired GLA production results in diminished synthesis of prostaglandin E1 (PGE1) in patients with AD, which, in turn, contributes to immune dysregulation and the development of dermatitis [84]. Blackcurrant seed oil, rich in EFAs, can effectively change the imbalance of EFAs in the body and temporarily reduce the prevalence of AD [11]. Chung et al. [85] identified EPO as a natural source of LA and GLA. The ingestion of GLA from EPO prompts an anti-inflammatory response by increasing the concentrations of GLA and DGLA in the bloodstream, which directly feed into the LA metabolic pathway, thereby gradually restoring anti-inflammatory PGE1 in the body, ultimately treating AD Foster et al. [83] found that borage essential oil typically comprises approximately 35–40% LA and 22–24% GLA. Supplementation with GLA increases DGLA levels, which increase the production of the anti-inflammatory mediator PGE1 in the skin. GLA exhibits antimicrobial properties, inhibiting the activity of S. aureus, which colonizes the skin. EFAs play a pivotal role in the skin’s structural integrity; therefore, supplementing with EFAs can serve as a complementary therapy for AD.

3.4. Essential oils reduce itching and relieve AD

Itching is a hallmark symptom of AD and is often regarded as a protective physiological response designed to shield the body from external damage. Surveys indicate that intense itching is prevalent in most patients with AD and is often the most distressing symptom. AD progression is associated with elevated production of inflammatory factors that stimulate mast cells, trigger IgE-mediated histamine release, and activate inflammatory pruritogens, which contribute to the sensation of itching [86,87]. The presence of pruritus initiates the itch-scratch cycle, where scratching in response to itching exacerbates inflammation and further damages the skin barrier, facilitating the penetration of pruritogens and antigens. This, in turn, activates keratin-forming cells, intensifying the itch and leading to additional skin damage [88]. Repeated cycles of itching and scratching result in the release of inflammatory cytokines such as IL-31 and thymic stromal lymphopoietin (TSLP), as well as chemokines like CCL2 and CXCL1, which activate pathogenic leukocytes, contributing to the development of skin lesions [89].

Essential oils are increasingly recognized for their efficacy in alleviating pruritus. Zhang et al. [90] demonstrated that the volatile oil of Cnidii Fructus, analyzed through gas chromatography-mass spectrometry (GC-MS) and network pharmacology, exerts its antipruritic effects via multi-component, multi-target, and multi-pathway mechanisms. Geraniol, a naturally occurring non-cyclic monoterpene found in essential oils such as rose, clove, and lemongrass oils, was studied by Yang et al. [91]in a model of acute itching, where chloroquine or compound 48/80 was intradermally injected into mice with shaved necks, and scratching behavior was recorded. Additionally, a chronic itching model was established through skin drying, and scratching behavior was continuously monitored. The results indicated that Geraniol effectively blocked gastrin-releasing peptide (GRP)-induced itching, inhibited DCP-induced upregulation of spinal GRP receptors (GRPR), and significantly reduced itching symptoms following intraperitoneal and intrathecal injections. These findings suggest that Geraniol may exert direct antipruritic effects at spinal cord segments, with the GRP-GRPR signaling pathway playing a role in itch relief. Topical application of peppermint essential oil has also proven effective for chronic pruritus, offering ease of use, safety, affordability, and high user acceptability [92]. When applied topically, peppermint essential oil stimulates cold receptors in nerve endings, triggering a cold sensation and subsequent vascular changes in deeper tissues, thereby relieving itching and exerting anti-inflammatory effects. Experimental studies on exopolysaccharides-peppermint oil (EPS-PO) emulsion, using phosphate histamine to induce itching in guinea pigs, showed that the EPS-PO emulsion significantly raised the itching threshold and reduced the frequency of scratching events [93]. Furthermore, aromatherapy massage with essential oils has been clinically shown to reduce itching and stress in older women [94]. These findings underscore the promising potential of essential oils in the future management of pruritic symptoms.

4. Essential oil monomers for AD

Essential oils used in the treatment of AD, with their monomers as the primary active constituents, can be classified into three major groups: monoterpenes, sesquiterpenes, and other compounds. As shown in Table 3, eleven monoterpenes, three sesquiterpenes, and two additional compounds have demonstrated significant therapeutic efficacy in mitigating skin inflammation. The structural formulas of these compounds have been presented in Figure 4.

Table 3. Classification of essential oil monomers for the treatment of AD (Increase, ↑; Decrease, ↓).

Categorization	Compound name	Types	Dose/concentration	Animal model	Effects/Mechanisms	References
Monoterpenes
	Thymol	In vivo	26 μL/pc Once a day; Successive 29 days;	DNCB-induced AD model	All inflammatory cells in the blood↓; mRNA expression levels of IL-4, IL-5 and IFN-γ↓;	[95,41]
	Carvacrol	In vivo	50 mg/kg	12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ear oedema	The release of inflammatory mediators↓;	[96]
	Perillyl alcohol	In vivo	6 mg/kg 12 mg/kg	TPA-induced skin oedema	The Ras/Raf/ERK pathway induces apoptosis in Swiss albino mouse skin↓;	[97]
	Linalyl acetate	In vivo	12.5, 25, 50 and 75 mg/kg	Carrageenan-induced oedema model in rats	The mechanism is unclear.	[98]
	p-Menthadienol	In vivo	0.1, 0.3, and 1.0%	Acute dermatitis model	TPA-induced skin inflammation↑; pro-inflammatory mediators IL-6↓; TNF-α↓;	[49]
	Citral	In vitro	3–12 μg/mL	LPS-stimulated RAW 264.7 cells	NO production↓; NF-κB activation↓;	[99]
	Limonene	In vivo	1.78-2.11 g/d	2,4-Dinitrofluorobenzene (DNFB) sensitization	NO production↓; IFN-γ↓; IL-4 production↓;	[100]
	p-Menthone	In vivo	0.1, 1, 10 μM/pc Once a day; Successive 19 days;	DNCB-induced AD model	IL-4↓; IFN-γ↓; inflammation↓; allergic responses↓;	[101]
	2,7-Dimethyl-2,6-octadiene	In vivo	50, 100, and 200 mg/kg	Diphenylcyclopripenone (DCP)–induced allergic contact dermatitis model	Chronic itch induced by DCP and AEW↓; GRPR expression in the spinal cord of DCP mice↑;	[102]
	L-menthol	In vivo	2.5 μg/μL; Once a day; Successive 7 days;	IMQ-induced skin inflammation	Protein phosphatase 6 in keratinocytes↓;	[103]
Sesquiterpene
	trans-Caryophyllene	In vivo	1 mg/kg	Carrageenan gum-induced paw oedema in rats	Release of TNF-α↓;	[104]
	α-caryophyllene	In vivo	1 mg/kg	Carrageenan gum-induced paw oedema in rats	TNF-α↓; IL-1β↓;	[104]
	Farnesol	In vivo	25, 50 and 100 mg/kg	TPA-induced skin oedema	TPA-induced skin oedema↓;	[97]
	β-Caryophyllene	In vivo	0.01,0.1,100 μg/mL	DNCB-induced AD model	MAPK ↓; the MAPK/EGR1/TSLP signaling axis↓;	[105]
Nitrocompounds
	1-Nitro-2-Phenylethylene	In vivo	0.9 mg/kg	LPS-induced pleurisy model	Neutrophil accumulation↓; NF-κB and ERK1/2 pathway activation↓;	[106]
Phenylpropanoid
	Cinnamaldehyde	In vivo	50 mg/kg	Dinitrofluorobenzene (DNFB)-induced dermatitis model in mice	IL-33↓; IL-25↓; cysteine-3 activities↓;	[107]
Coumarins
	Osthole	In vivo	5, 25,50 mg/kg	DNCB-induced AD model	Scratching bouts↓; p-p65↓; PPARγ↑; PPARα↑;	[108]

Structural formulae of monomer compounds for the treatment of AD.

4.1. Monoterpenes

4.1.1. Linalool

Linalool, a linear monoterpene commonly found in essential oils such as basil, bergamot, sage, coriander, lavender, neroli, and nutmeg, is a prominent floral fragrance compound known for its anti-inflammatory, sedative, and anxiolytic properties [109]. Classified by the US Food and Drug Administration as a generally recognized as safe (GRAS) substance, linalool has been shown to exhibit a pro-osmotic effect, enhancing drug penetration into the skin. It is frequently encountered as an anti-inflammatory agent in various essential oils. In animal studies, intraperitoneal injection of α-pinene or linalool in mice has been shown to inhibit COX-1 and provide pain relief, as well as demonstrating anti-inflammatory effects in carrageenan-induced paw edema models. In BALB/c mice with an imiquimod (IMQ)-induced psoriasis model, topical application of linalool, alongside in vivo anti-psoriasis assays, immunohistochemical analysis, and skin irritation studies, demonstrated its effectiveness in treating IMQ-induced psoriasis (including skin inflammation), establishing a basis for the topical use of lavender essential oil (LEO) [110]. Furthermore, linalool, as a primary monomer in essential oils, has been shown to target retinoid-related orphan nuclear receptor γt, reducing the production of inflammatory factors such as TNF-α and IL-17A. This mechanism contributes to the alleviation of skin symptoms in DNCB-induced dermatitis models [111]. In summary, existing studies highlight the broad therapeutic potential of linalool in addressing skin inflammation, positioning it as a promising candidate for future drug development in the treatment of inflammatory skin diseases.

4.1.2. α-Pinene

α-Pinene is a typical monoterpene, the most prevalent naturally occurring hydrocarbon. It is present in various essential oils, such as cypress, eucalyptus blue, fennel, lavender, pine, rosemary, tea tree, frankincense, and other plant-derived essential oils. This compound exhibits a broad spectrum of pharmacological activities, including antimicrobial, antioxidant, anti-inflammatory, modulation of antibiotic resistance, anticoagulant, and antitumor effects [112]. α-Pinene, the primary constituent of rosemary essential oil, plays a significant therapeutic role in disease treatment. Rosemary essential oil has been shown to significantly improve skin symptoms in a DNCB-induced dermatitis mouse model. Its primary component, α-pinene, acts on the JAK target proteins to regulate the JAK/STAT/NF-κB pathway and reduce the production of inflammatory mediators, thus improving skin symptoms. Furthermore, α-pinene exhibits significant anti-inflammatory activity, as evidenced by its efficacy in carrageenan or prostaglandin E (PGE)-induced rat hind paw edema models and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ear edema [113]. α-Pinene, a prominent constituent found in Boswellia serrata oil, Chiba oil, and Trigonella oil, has demonstrated inhibitory effects on edema formation induced by carrageenan and PGE1. Additionally, it significantly alleviates symptoms associated with TPA-induced ear edema in rat paw edema tests [114]. Numerous studies have delved into the impact of monomeric α-pinene on the skin. Skin photoaging test involving UVA-irradiated mouse skin has demonstrated that a-pinene effectively. Skin photoaging test involving UVA-irradiated mouse skin has demonstrated that α-Pinene effectively mitigates UVA-induced photoaging by inhibiting the expression of the inflammatory factors TNF-α and IL-6, as well as the activation of NF-κB and p65 in mouse skin [115]. In vitro, α-pinene has been shown to exert a protective effect on UVA-induced epidermal keratinocytes (HaCaT cells) in human skin, significantly reducing the production of inflammatory mediators (NF-κB, TNF-α) in HaCaT cells [116]. These findings underscore the robust anti-inflammatory potential of α-pinene, making it a promising candidate for the treatment of inflammatory skin diseases.

4.1.3. Linalyl acetate

Linalyl acetate is a monoterpene lipid compound primarily found in bergamot, sage, jasmine, lavender, lemon, and neroli essential oils, as well as other essential oils. Linalyl acetate is the primary fragrance component in flavor preparations. It is chemically stable and finds extensive utilization in shampoos, detergents, cosmetics, and edible flavored teas. Studies have revealed several pharmacological properties of Linalyl acetate, such as anti-inflammatory, antioxidant, analgesic, and antispasmodic effects. Moreover, Linalyl acetate can be used to treat diseases such as endothelial dysfunction, psoriasis, and AD [117]. Linalyl acetate has demonstrated its efficacy in the treatment of psoriasis. In vitro anti-inflammatory activity assays involving lipopolysaccharide (LPS)-induced macrophages have indicated that Linalyl acetate significantly inhibits the expression levels of TNF-α and IL-6. Furthermore, in vivo experiments involving BALB/c mice with IMQ-induced psoriasis have shown that Linalyl acetate not only improves body weight but also significantly alleviates skin erythema and reduces NF-κB expression [118]. In response to network pharmacology, molecular docking predictions indicate that Linalyl acetate, a major component of LEO, in the treatment of DNCB-induced dermatitis, primarily exerts its effects on the IL-6 target protein in the Th17 cell pathway. This action influences the expression of p-STAT3, which inhibits Th17 cell differentiation, thereby reducing the production of inflammatory factors and ultimately improving skin symptoms [111]. In an inflammatory rat model, Linalyl acetate was shown to prevent vascular endothelial dysfunction and mitigate cardiovascular disease-induced endothelial dysfunction by regulating intracellular calcium levels in endothelial cells [119]. These studies collectively suggest that Linalyl acetate exerts a significant ameliorative effect on skin inflammation, thereby presenting potential avenues for the development of novel therapies for skin inflammation.

4.2. Sesquiterpenes

α-Bisabolol (BISA), also known as levomethanol, is a natural monocyclic sesquiterpene compound primarily found in German chamomile, spring chamomile essential oils, and other essential oils. Particularly in Matricaria chamomilla essential oils, its concentration can reach up to 50%. BISA is a transparent, colorless liquid possessing a fruity, nutty fragrance reminiscent of coconut and exhibits favorable physicochemical properties [120]; thus, it is utilized as a fragrance ingredient. Due to its skin-soothing and healing properties, BISA has garnered significant attention for its incorporation into numerous cosmetic formulations as a soothing cosmetic additive. This compound has found applications in cosmetics, chemistry, and pharmaceuticals [121]. BISA exhibits a wide array of biological activities, including antioxidant, anti-inflammatory, gastroprotective, anti-infective, and anticancer properties. Its significant anti-inflammatory effects suggest potential utility in mitigating inflammation induced by Collagen Induced Arthritis. This effect is achieved through the inhibition of proteases and inflammatory mediators, rendering BISA a potential candidate for combating inflammation in arthritis [122]. Moreover, using erythromycin, designed for the treatment of acute eczematous conditions such as nappy dermatitis (DD), BISA has been shown to have a significant impact on skin-related disorders. However, this formulation may also be particularly suitable for AD. To assess the effectiveness and tolerability of this cream, a six-week, three-center, evaluator-blinded prospective treatment trial involving children with chronic mild to moderate AD was conducted. This trial provided compelling evidence supporting the efficacy and tolerability of a corticosteroid-free cream containing red myrcene for the treatment of chronic mild to moderate AD in children [123,124]. In vitro and in vivo assays have demonstrated the therapeutic effect of BISA on skin inflammation; BISA significantly inhibits LPS and TPA-induced pro-inflammatory production of cytokines (TNF-α and IL-6) in macrophages, as well as TPA-induced skin inflammation in mice. Moreover, the topical application of BISA significantly suppressed TPA-induced ear thickening, ear weight, lipid peroxidation, histopathological alterations, and ear tissue damage in a dose-dependent manner. Both in vitro and in vivo toxicity profiles indicate that topical application to the skin is safe. Molecular docking studies have revealed a robust binding affinity for the active sites of pro-inflammatory proteins. These findings suggest that BISA represents a promising candidate for the treatment of skin inflammation [125]. Furthermore, BISA has been shown to effectively ameliorate skin symptoms in a mouse model of DNCB-induced dermatitis and alleviate AD by inhibiting the activation of c-Jun N-terminal kinase and NF-κB in mast cells and reducing inflammatory cytokines [126]. These findings suggest that BISA holds significant potential as a therapeutic agent for AD and other mast cell-related diseases.

4.3. Other categories

4.3.1. Eugenol (EUG)

EUG is a phenylpropanoid compound primarily derived from essential oils found in basil, black pepper, cinnamon leaves and buds, cloves, nutmeg, and other sources. It is a clear to pale yellow liquid with an oily consistency and a pungent aroma at room temperature. EUG is slightly soluble in water but highly soluble in organic solvents. Known for its broad spectrum of biological activities, including anti-inflammatory, antimicrobial, antioxidant, anti-asthmatic, and insecticidal properties, EUG has been widely utilized in pharmaceuticals, flavorings, and cosmetics [127,128]. EUG’s antimicrobial efficacy extends to various bacterial pathogens, including S. aureus, Pseudomonas aeruginosa, and Escherichia coli. The compound’s primary mechanism of action involves the free hydroxyl groups in its structure, which disrupt cytoplasmic membranes. As a hydrophobic molecule, EUG can easily penetrate lipopolysaccharide cell membranes, entering the cytoplasm and inducing structural alterations in cells, leading to leakage of intracellular components [129]. Furthermore, EUG has demonstrated significant anti-inflammatory effects, particularly in the context of treating inflammatory diseases. In studies involving TPA- and 7,12-dimethylbenz[a]anthracene-induced skin tumor models, EUG inhibited pro-inflammatory cytokines (IL-6, TNF-α, and PGE2) and upstream signaling molecules like NF-κB, resulting in a marked preventive effect on inflammation [130]. Additionally, EUG exhibits pro-osmotic properties, enhancing transdermal drug absorption and promoting a reduction in pleural volume in mice with carrageenan-induced inflammation. It also inhibits pro-inflammatory mediators such as COX-2, NF-κB, and IL-6. EUG derivatives have been shown to exhibit anti-inflammatory activity in ex vivo models of skin inflammation [131]. Given the increasing interest in traditional medicines incorporating natural compounds, EUG holds considerable promise as an active ingredient in therapeutic products, particularly those targeting skin inflammation.

4.3.2. 1-Iodohexadecane

1-Iodohexadecane, an alkyl compound found in the essential oil of chrysanthemum, possesses antibacterial, antioxidant, and anticancer properties, as well as other pharmacological properties. This constituent has been shown to inhibit dermatitis-like lesions, and in atopic diseases, such as AD, it may be associated with mast cells, which are a significant effector in atopic diseases. Studies indicate that 1-iodohexadecane inhibits histamine and β-hexosaminidase release in mast cells induced by IgE. In DNCB-treated mice, 1-iodohexadecane demonstrated ameliorative effects on AD-like skin lesions, reducing epidermal thickness, mast cell infiltration, and increasing the expression of filamentous polyproteins and skin barrier proteins. These findings suggest that 1-iodohexadecane may ameliorate the severity of AD lesions by either disrupting soluble N-ethylmaleimide-sensitive factor attachment protein receptor protein junctions responsible for degranulation or enhancing the expression of skin barrier-associated proteins. Consequently, 1-iodohexadecane holds therapeutic potential for the treatment of AD [40]

5. Comparison of conventional medications for AD with natural plant essential oils

Most natural plant essences exhibit a range of biological activities, including anti-inflammatory properties (e.g., cinnamon essential oil [132], LEO [111], frankincense essential oil [133], rosemary essential oil [134]) and antimicrobial effects (e.g., basil essential oil, peppermint essential oil, oregano essential oil, spearmint essential oil [135]). The progression of AD is often accompanied by infections caused by pathogenic bacteria, such as S. aureus or Staphylococcus epidermidis, and elevated levels of inflammatory cytokines. Consequently, the primary therapeutic focus for AD has been on antimicrobial and anti-inflammatory treatments. However, conventional commercially available medications present various limitations.

Currently, AD treatment primarily involves topical agents, with systemic medications reserved for more severe cases. Most of the available drugs for AD are anti-inflammatory agents that exert their therapeutic effects by reducing inflammatory cytokines and suppressing the inflammatory response. Topical corticosteroids and calcium-modulated phosphatase inhibitors are commonly used for mild to moderate AD. For severe, long-term cases, treatments may include JAK inhibitors, phosphodiesterase inhibitors, biologics, or immunosuppressants, all of which carry notable side effects [2]. In contrast, ginger essential oil (GEO) provides an alternative approach by significantly modulating inflammatory factors to attenuate skin inflammation. The anti-inflammatory effects of GEO on the skin were validated in three animal models: the carrageenan-induced skin inflammation model, the xylene-induced ear swelling model in mice, and the 2,4-dinitrofluorobenzene-induced ear swelling mode [136]. While essential oils may not act as rapidly as chemotherapeutic drugs, they offer relative safety, reliability, and a reduced risk of harm to the human body. As S. aureus remains a major pathogen associated with AD and often contributes to secondary infections, essential oils may serve as a promising adjunct or alternative treatment option in managing this condition. Several antimicrobial drugs, such as mupirocin and fusidic acid, are commonly used in the treatment of AD. These antimicrobials are typically applied topically to minimize systemic toxicity and adverse effects. However, prolonged use of these drugs can lead to the development of drug-resistant bacterial strains, complicating the management of the condition [137]. The antimicrobial activity of essential oils primarily stems from their active components, some of which can penetrate cell membranes to target pathogenic bacteria, while others influence membrane permeability, disrupting cellular integrity [138]. For instance, fir essential oil has shown significant antimicrobial activity against acne-causing bacteria such as Propionibacterium acnes and S. epidermidis, as demonstrated through antimicrobial assays [139]. Compared to conventional antimicrobial drugs, essential oils often exhibit superior antimicrobial properties, preventing pathogens from invading the body and helping to reduce the risk of secondary infections.

This article offers a comparative analysis of conventional drugs and essential oils for AD treatment, focusing on their anti-inflammatory and antibacterial properties (Table 4). Research indicates that conventional drugs provide a rapid onset of action and high efficacy, delivering short-term relief from AD symptoms and improving patients’ quality of life. However, these drugs come with notable drawbacks, including side effects that can lead to long-term damage with prolonged use. While newer biologic therapies offer reduced side effects and improved efficacy, they are costly and may not be a cost-effective solution. In contrast, essential oils present a promising alternative with superior anti-inflammatory and antibacterial properties, alongside other beneficial biological activities. They are characterized by their safety, rapid absorption, minimal side effects, and precise therapeutic effects. However, the quality of essential oils on the market varies widely. Low-quality or impure essential oils not only fail to deliver therapeutic benefits but may also pose potential health risks. Future studies could investigate the synergistic effects of essential oils in combination with traditional medicines, which may enhance efficacy and provide better treatment outcomes for AD.

Table 4. Comparison of existing drugs and essential oils for AD.

Category	Treatments	Therapeutic effect	Side effect	Mechanism	References
conventional treatments	Hormone-type drug (Hydrocortisone, triamcinolone acetonide, mometasone furoate, etc.)	It relieves itching and controls inflammation;	Recommended for short-term or intermittent use only Adverse skin reactions limit long-term use (e.g. streaking, skin atrophy, capillary dilatation)	By inhibiting the inflammatory pathway mediates the anti-inflammatory effect and promotes the reduction of inflammation	[140]
	Calcium-modulated phosphatase inhibitor (Tacrolimus, pimecrolimus)	Avoid recurring inflammation over time	Causes a transient burning sensation at the site Long-term continuous use Concerns about malignant tumors	It disrupts IL-2 activity and interferes with T cell activation, proliferation and differentiation	[141]
	Anti-infective drugs (Mupirocin, fusidic acid)	Can avoid secondary bacterial infections such as Staphylococcus	Prolonged use can create resistance and even cause secondary infections.	Inhibit the synthesis of bacterial cell walls	[137]
	Antihistamine (Loratadine, Ebastine)	Avoid damaging the skin barrier function by excessive scratching;	Non-sedating antihistamines have little effect on symptoms	Effectively blocks histamine binding to H₁ receptors in skin and other peripheral tissues	[83]
	Biological agents or immunosuppressants (Cyclosporine, azathioprine, methotrexate, dupliyuzumab)	Comprehensively inhibits and relieves the skin’s inflammatory response.	Rebound/relapse on discontinuation of therapy Long-term use limited by serious adverse effects	Inhibit T cell proliferation and regulate immune response by inhibiting purine synthesis.	[142]
	Janus kinase inhibitor (Baricitinib, Tofacitinib)	Blocking a wide range of signaling involved in the immune response and inflammatory factors has shown promising therapeutic effects in AD.	Prolonged use may cause adverse side effects such as nausea, diarrhea, and elevated cholesterol.	By selectively inhibiting the JAK enzyme, the downstream STAT signaling is blocked and the expression of cytokines involved in the pathogenesis of AD is prevented	[143,144]
Essential oil	Essential oil	It has good anti-inflammatory, antibacterial and antipruritic effects, Repair skin dysfunction	Presence of skin irritation Allergic reaction Respiratory irritation	Regulate inflammatory factors and pathways to reduce inflammatory response Supplement with EFAs to relieve the symptoms of dermatitis	[145]

6. Clinical trials of natural medicinal essential oils for dermatitis treatment

The clinical presentation of AD varies in severity, influenced by factors such as erythema, exfoliation, and the presence of lichen planus, which can affect its clinical diagnosis. According to the latest guidelines from the American Academy of Dermatology, the presence of itching and eczema is essential for diagnosing AD. However, additional factors, including early age of onset and a genetic history of allergies, also contribute to the diagnosis. The development of AD is frequently associated with various complications, such as allergic rhinitis, asthma, and food allergies, which significantly impact both physical and mental health [146].

Blackcurrant (Ribes nigrum) seed oil (BCSO), rich in EFAs such as n-6 fatty acids, gamma-linolenic acid (GLA), stearic acid, and oleic acid, may influence the prevalence of AD when used as a dietary supplement. A double-blind, placebo-controlled clinical trial involving 313 pregnant women, randomized to receive either BCSO (151 participants) or olive oil as a placebo (162 participants), assessed AD severity using the SCORing Atopic Dermatitis (SCORAD) index, serum total IgE levels, and skin tests. Results indicated that the BCSO group experienced a reduction in AD prevalence in 12-month-old infants compared to the placebo group, suggesting that BCSO may temporarily decrease AD incidence [11]. Diaper dermatitis (DD), a common skin disorder in young children, was also addressed in clinical trials using argan oil. Rich in linoleic acid (LA), argan oil has demonstrated therapeutic effects in various inflammatory skin conditions, including acne and chickenpox. A clinical trial involving 147 children, randomized to receive either argan oil (73 participants) or 1% hydrocortisone ointment (74 participants), evaluated healing and improvement rates through home visits. The study concluded that argan oil was more effective than 1% hydrocortisone in treating DD and could also be considered a treatment option for acne. However, cortisone proved to be more effective and could be used as a complementary therapy [147].

EPO, rich in EFAs such as GLA and DGLA, has been shown to alleviate the symptoms of AD when supplemented. A study assessed the effects of daily EPO administration over 12 weeks in 21 patients with AD, using the SCORAD index for evaluation. Gas chromatography was employed to measure plasma GLA and DGLA levels, along with IgE levels. Results indicated a significant reduction in the SCORAD index following EPO treatment, with a negative correlation between GLA levels and the SCORAD index, suggesting that higher GLA levels were associated with greater improvement in dermatitis. These findings support the potential of EPO supplementation in alleviating skin symptoms in patients with AD [148]. Borage oil, containing 2–3 times the EFAs found in EPO, has also been extensively studied for AD management. In a double-blind clinical trial involving 160 patients with AD, participants were randomly assigned to receive either borage oil or a placebo (miglyol) for 24 weeks, with various intervals and Costa scores recorded, and plasma IgE levels assessed. The results indicated that borage oil is a beneficial food supplement for relieving AD symptoms. However, while borage oil is generally well tolerated in the short term, long-term tolerance data remain unavailable [83]. In clinical practice, essential oils primarily serve as complementary therapies. Given that chronic EFA deficiency can contribute to AD, essential oils rich in EFAs are increasingly utilized to alleviate AD symptoms.

7. Conclusions and perspectives

AD is an inflammatory skin disorder characterized by skin lesions and intense itching. Its pathophysiology involves a combination of genetic and environmental factors, microbial immune imbalances, barrier dysfunction, and immune dysregulation. Essential oils and their active constituents can provide effective therapeutic outcomes in AD by mechanisms such as inhibiting S. aureus colonization, supplementing EFAs, modulating inflammatory cytokines, and influencing key signaling pathways. Conventional AD treatments primarily rely on topical anti-inflammatory and analgesic medications, including corticosteroids, calmodulin phosphatase inhibitors, and topical antibiotics or anti-infectives to prevent microbial infections. However, prolonged use of these drugs can lead to drug resistance and severe side effects. Natural plants, particularly in developing countries like China, remain a major source of medicinal resources, with plant-based medicines playing a central role in traditional healing practices. Essential oils, as vital components of these plants, are often considered safe and effective for use as complementary or alternative therapies in AD treatment, helping to reduce adverse effects while enhancing therapeutic efficacy. To ensure the responsible development of the essential oils market, it is crucial to establish robust regulations and policies to govern their use and promote safe practices.

Essential oils have demonstrated significant efficacy and widespread clinical application in treating skin disorders. Numerous natural plant essential oils have undergone clinical trials, revealing their antibacterial, antioxidant, anti-inflammatory, antidepressant, and antipruritic properties. These trials have demonstrated that the synergistic effects of compound essential oils can effectively restore the skin’s hydrolipidic balance and maintain optimal skin morphology. This review examined the therapeutic potential of essential oils in treating dermatitis, highlighting their favorable clinical benefits. One of the pathogenic mechanisms of AD is the deficiency of EFAs, which exacerbates severe skin symptoms. Essential oils rich in EFAs are commonly used in topical treatments to replenish depleted EFAs and improve skin condition in patients with AD. To maximize the pharmacodynamic effects of essential oils, novel formulations incorporating micro- and nanocarrier systems should be explored. Such formulations can enhance drug efficacy, improve patient compliance, and reduce adverse effects. Essential oils, being lipophilic with limited aqueous solubility, present significant formulation challenges, particularly for aqueous-based systems like topical creams, lotions, and oral suspensions. Additionally, their volatility and susceptibility to oxidation may lead to the degradation of bioactive compounds, diminishing therapeutic efficacy over time. Existing studies indicate a gap in research on these issues. However, research on essential oils is still lacking in areas such as safety and toxicity assessments. Essential oils are typically administered as oil solutions or incorporated into topical preparations, which can sometimes cause skin irritation, erythema, and allergic reactions. While topical application is generally safe for certain essential oils, higher doses or ingestion may lead to skin irritation and contact sensitization. LEO causes mild irritation when applied topically at a 10% concentration, while linalool and LA exhibited non-irritating properties when applied at a 2% concentration. Moreover, a significant proportion of individuals may experience allergic reactions to certain components in essential oils, leading to contact dermatitis or other adverse allergic responses.

Given these considerations, it is crucial to incorporate modern and emerging disciplines, along with advanced experimental methodologies, for a comprehensive and systematic exploration of the mechanisms underlying the therapeutic effects of essential oils in treating AD. Future research could apply molecular distillation technology to isolate distinct components of essential oils based on their boiling points, thereby enhancing the concentration of active components and removing ineffective ones, ensuring both efficacy and safety. The combination of different essential oils, or their integration with other bioactive compounds, may yield synergistic effects that enhance overall therapeutic efficacy. For example, a combination of Artemisia campestris and Citrus aurantium essential oils has demonstrated stronger anti-inflammatory activity than either oil alone. However, identifying optimal combinations and understanding the underlying synergistic mechanisms remain in the early stages of research. Integrating essential oils into novel formulations and developing advanced delivery systems represents a promising area for further investigation. Nanotechnology-based methods, such as nanoemulsions, liposomes, and solid lipid nanoparticles, are expected to improve the solubility, bioavailability, and targeted delivery of essential oils, thereby enhancing their therapeutic potential. Despite the increasing use of essential oils across various applications, the mechanisms underlying their biological activities remain incompletely understood. Further in-depth studies are necessary to elucidate how essential oils interact with biological systems at the molecular and cellular levels. Such research could reveal additional therapeutic targets for specific forms of dermatitis and expand possibilities for future investigations.

Acknowledgment

The authors gratefully acknowledge the financial supports by the National Key Research and Development Program of China ( 2021YFD1601004, 2023YFD1600402, 2023YFD1600403); Shaanxi Provincial Key Research and Development Program Project (2024CY-JJQ-36); Xi’an Science and Technology Plan Project (20231H-JSJ0-0007); Inner Mongolia Autonomous Region Science and Technology Program (2022YFSH0001); Science and Technology Programmer of Xixian New Area (DJK-2023-004); Shaanxi Provincial Traditional Chinese Medicine Science and Technology Innovation Team (TZKN-CXTD-03); Shaanxi Provincial Department of Science and Technology Project (2024 ZC-YYDP-110); Shaanxi Province Xianyang City Science and Technology Bureau Project (L2024-QCY-ZYYJJQ-X28); Shaanxi Provincial Administration of Traditional Chinese Medicine (ZYJXG-Y23005); National-Level High-Caliber Talent Innovation and Entrepreneurship Project; Key Technological Innovation Team for Industrialization of Aromatic Traditional Chinese Medicine; Engineering Research Center of Traditional Chinese Shaanxi Medicine Aromatic Industry, Universities of Shaanxi Province, Key Discipline of High Level Traditional Chinese Medicine in Shaanxi Province, Traditional Chinese Medicine Processing.

CRediT authorship contribution statement

Jiawei Duan, Xiaofei Zhang, and Fei Luan drafted the manuscript. Jinkai Li, Junbo Zou, Jing Sun, Yajun Shi, and Xiao Wang made critical revisions and gave suggestions during the preparation. Changli Wang and Dongyan Guo prepared the figures. All authors listed gave final approval for publication.

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Declaration of Generative AI and AI-assisted technologies in the writing process

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

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1. Introduction

2. Pathogenesis of AD

2.1. Genetic and environmental factors
2.2. Skin barrier dysfunction
2.3. Microbial ecological imbalance
2.4. Immune dysfunction

3. Advancements in essential oil research for AD treatment

3.1. Inhibition of S. aureus colonization by essential oils

3.2. Essential oils reduce inflammation by modulating relevant inflammatory factors and pathways
3.3. Essential oils complement EFAs in alleviating AD
3.4. Essential oils reduce itching and relieve AD

4. Essential oil monomers for AD

4.1. Monoterpenes
4.2. Sesquiterpenes
4.3. Other categories

5. Comparison of conventional medications for AD with natural plant essential oils

6. Clinical trials of natural medicinal essential oils for dermatitis treatment

7. Conclusions and perspectives

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Therapeutic role of essential oils in atopic dermatitis: A review

Abstract

Keywords

Atopic dermatitis

Essential oil

Mechanism

Monomer

Pathogenesis

1. Introduction

2. Pathogenesis of AD

2.1. Genetic and environmental factors

2.2. Skin barrier dysfunction

2.3. Microbial ecological imbalance

2.4. Immune dysfunction

3. Advancements in essential oil research for AD treatment

3.1. Inhibition of S. aureus colonization by essential oils

3.2. Essential oils reduce inflammation by modulating relevant inflammatory factors and pathways

3.3. Essential oils complement EFAs in alleviating AD

3.4. Essential oils reduce itching and relieve AD

4. Essential oil monomers for AD

4.1. Monoterpenes

4.1.1. Linalool

4.1.2. α-Pinene

4.1.3. Linalyl acetate

4.2. Sesquiterpenes

4.3. Other categories

4.3.1. Eugenol (EUG)

4.3.2. 1-Iodohexadecane

5. Comparison of conventional medications for AD with natural plant essential oils

6. Clinical trials of natural medicinal essential oils for dermatitis treatment

7. Conclusions and perspectives

Acknowledgment

CRediT authorship contribution statement

Declaration of competing interest

Declaration of Generative AI and AI-assisted technologies in the writing process

References

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