4.7 Article

Oleanolic Acid Alleviates Atopic Dermatitis-like Responses In Vivo and In Vitro

Journal

Publisher

MDPI
DOI: 10.3390/ijms222112000

Keywords

oleanolic acid; atopic dermatitis; 2,4-dinitrochlorobenzene; keratinocyte; NF-kappa B; STAT1

Funding

  1. National Research Foundation of Korea (NRF) [NRF-2017R1C1B2008617, NRF-2017M3A9B6061511]
  2. Sangji University Graduate School
  3. National Research Foundation of Korea [2017M3A9B6061511] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Oleanolic acid (OA) exhibits anti-atopic effects by suppressing AD-like lesions and regulating inflammatory mediators, suggesting its potential as a therapeutic agent for allergic disorders such as atopic dermatitis (AD). The inhibitory effects of OA on Th2 cytokines and chemokines in AD mouse model and keratinocytes were mediated through blocking the activation of key signaling pathways. These findings provide novel insights into the pharmacological targets of OA for treating AD.
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)-alpha/interferon (IFN)-gamma-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-alpha/IFN-gamma-induced HaCaT keratinocytes by blocking the activation of serine-threonine kinase Akt, nuclear factor-kappa B, 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.

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