Korean Medicine Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu 41062, Korea.
ViroMed Co., Ltd., Seoul National University 1, Gwanak-ro, Gwanak-gu, Seoul 151-747, Korea.
Nutrients. 2018 Jun 22;10(7):806. doi: 10.3390/nu10070806.
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 Hance in atopic dermatitis (AD) are not fully understood. An ethanolic extract of 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 (IκB-α) in TNF-α/IFN-γ⁻stimulated HaCaT cells. EAH also suppressed the translocation of inflammation transcription factors such as NF-κB p65 in TNF-α/IFN-γ⁻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-κB pathways. Furthermore, EAH significantly improved the skin p38 conditions in a DNCB-induced AD-like mouse model.
岗梅是一种传统的中草药，在中国、韩国和日本等东亚国家用于治疗湿疹和黄疸。然而，岗梅在特应性皮炎（AD）中的生物和药理作用尚不完全清楚。岗梅的乙醇提取物（EAH）在体外和体内进行了测试，以研究其抗炎活性和抗特应性皮炎作用。结果表明，EAH 呈剂量依赖性地抑制调节激活、正常 T 细胞表达和分泌（RANTES）、白细胞介素（IL）-6、IL-8 和胸腺激活调节趋化因子（TARC）的产生。EAH 抑制 p38、细胞外信号调节激酶（ERK）和 STAT-1 的激活，并抑制 TNF-α/IFN-γ⁻刺激的 HaCaT 细胞中核因子κ轻肽基因增强子 B 抑制剂-α（IκB-α）的降解。EAH 还抑制 TNF-α/IFN-γ⁻刺激的 HaCaT 细胞中炎症转录因子如 NF-κB p65 的易位。此外，EAH 以剂量依赖的方式减少了 2,4-二硝基氯苯（DNCB）诱导的耳部厚度和背部皮肤厚度。EAH 似乎通过抑制 ERK 和 NK-κB 途径的激活来调节趋化因子的形成。此外，EAH 显著改善了 DNCB 诱导的 AD 样小鼠模型中的皮肤 p38 状况。
