Abstract
Oleanolic acid (OA) is a pentacyclic triterpenoid, abundantly found in plants of the Oleaceae family, and is well known for its beneficial pharmacological activities. Previously, we reported the inhibitory effect of OA on mast cell-mediated allergic inflammation. In this study, we investigated the effects of OA on atopic dermatitis (AD)-like skin lesions and its underlying mechanism of action. We evaluated the inhibitory effect of OA on AD-like responses and the possible mechanisms using a 1-chloro-2,4-dinitrochlorobenzene (DNCB)-induced AD animal model and tumor necrosis factor (TNF)-α/interferon (IFN)-γ-stimulated HaCaT keratinocytes. We found that OA has anti-atopic effects, including histological alterations, on DNCB-induced AD-like lesions in mice. Moreover, it suppressed the expression of Th2 type cytokines and chemokines in the AD mouse model and TNF-α/IFN-γ-induced HaCaT keratinocytes by blocking the activation of serine-threonine kinase Akt, nuclear factor-κB, and the signal transducer and activator of transcription 1. The results demonstrate that OA inhibits AD-like symptoms and regulates the inflammatory mediators; therefore, it may be used as an effective and attractive therapeutic agent for allergic disorders, such as AD. Moreover, the findings of this study provide novel insights into the potential pharmacological targets of OA for treating AD.
Highlights
Allergic inflammation is characterized by pathophysiological or hypersensitivity disorders, including allergic asthma, allergic rhinitis, anaphylaxis, and atopic dermatitis (AD), after exposure to allergens [1]
To investigate the mechanism responsible for the inhibitory effect of Oleanolic acid (OA) in parallel with the inhibition of Nuclear factor (NF)-κB, we investigated its effect on tumor necrosis factor (TNF)-α/IFN-γ-induced STAT1 activation
The results demonstrated that the anti-inflammatory effects of OA in HaCaT and DNCB-induced AD mice are associated with the STAT1 signaling pathway
Summary
Allergic inflammation is characterized by pathophysiological or hypersensitivity disorders, including allergic asthma, allergic rhinitis, anaphylaxis, and atopic dermatitis (AD), after exposure to allergens [1]. AD is a chronic inflammatory skin disease that arises from the complicated interaction of innate and adaptive immune responses based on genetics, environmental factors, immune abnormalities, and skin barrier functions [2]. The characteristic features of AD include itchy, swollen, red, and cracked skin with inflammatory cell accumulation in AD skin lesions. Th2 cells are mainly activated in the acute phase of AD, while Th1 cells mediate the alteration of expression in chronic AD [3]. The standard treatment for AD involves the application of topical corticosteroids or the administration of immunosuppressive agents; protracted use of these agents can cause various side effects, such as skin atrophy, bleeding, vasodilation, and organ toxicity. Medicines originating from herbal sources may be preferred to steroids, and may be used in combination with other methods, such as enhancing immunity, reducing house mite dust, and dietary restrictions [4,5]
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