Ethanolic Extracts of Artemisia apiacea Hance Improved Atopic Dermatitis-Like Skin Lesions In Vivo and Suppressed TNF-Alpha/IFN-Gamma–Induced Proinflammatory Chemokine Production In Vitro

Abstract

<i>Artemisia apiacea</i> Hance is a traditional herbal medicine used for treating eczema and jaundice in Eastern Asia including China, Korea, and Japan. However, the biological and pharmacological actions of <i>Artemisia apiacea</i> Hance in atopic dermatitis (AD) are not fully understood. An ethanolic extract of <i>Artemisia apiacea</i> Hance (EAH) was tested in vitro and in vivo to investigate its anti-inflammatory activity and anti-atopic dermatitis effects. The results showed that EAH dose-dependence inhibited production of regulated on activation, normal T-cell expressed and secreted (RANTES), interleukin (IL)-6, IL-8, and thymus and activation-regulated chemokine (TARC). EAH inhibited the activation of p38, extracellular signal-regulated kinases (ERK), and STAT-1 and suppressed the degradation of inhibited both nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha (I&kappa;B-&alpha;) in TNF-&alpha;/IFN-&gamma;⁻stimulated HaCaT cells. EAH also suppressed the translocation of inflammation transcription factors such as NF-&kappa;B p65 in TNF-&alpha;/IFN-&gamma;⁻stimulated HaCaT cells. In addition, EAH reduced 2,4-dinitrochlorobenzene (DNCB)-induced ear thickness and dorsal skin thickness in a dose-dependent manner. EAH appeared to regulate chemokine formation by inhibiting activation of and ERK as well as the NK-&kappa;B pathways. Furthermore, EAH significantly improved the skin p38 conditions in a DNCB-induced AD-like mouse model.