Oh Chang Taek, Jang Yu-Jin, Kwon Tae-Rin, Im Songi, Kim Soon Re, Seok Joon, Kim Gun-Yong, Kim Young-Heui, Mun Seog Kyun, Kim Beom Joon
Department of Dermatology, Chung‑Ang University College of Medicine, Seoul 156‑755, Republic of Korea.
Department of Biotechnology R&D, SK Bioland Corporation, Cheongju, North Chungcheong ASI/KR/KS001, Republic of Korea.
Mol Med Rep. 2017 May;15(5):2681-2688. doi: 10.3892/mmr.2017.6306. Epub 2017 Mar 9.
The present study aimed to investigate the anti‑inflammatory effect and mechanism of action of isosecotanapartholide (ISTP), isolated from Artemisia princeps Pampanini extract (APE). The effects of ISTP and APE on the proliferation of human keratinocytes following stimulation by tumor necrosis factor‑α/interferon‑γ were assessed. ISTP and APE downregulated the expression levels of signal transducer and activator of transcription‑1 (STAT‑1), and reduced interleukin‑33 (IL‑33) production. ISTP and APE inhibited the mRNA expression levels of thymus and activation‑regulated chemokine (TARC/CCL17) in a dose‑dependent manner. Western blot analysis demonstrated that ISTP and APE dose‑dependently inhibited protein expression levels of intercellular adhesion molecule‑1 and phosphorylation of STAT‑1. The results of the present study indicate that ISTP may inhibit TARC/CCL17 production in human epidermal keratinocytes via the STAT‑1 signaling pathway and may be associated with the inhibition of IL‑33 production. The current study indicated that ISTP is an active component in APE and may be a potential therapeutic agent for the treatment of inflammatory skin disorders.
本研究旨在探讨从黄花蒿提取物（APE）中分离得到的异泽泻醇内酯（ISTP）的抗炎作用及其作用机制。评估了ISTP和APE对肿瘤坏死因子-α/干扰素-γ刺激后人角质形成细胞增殖的影响。ISTP和APE下调了信号转导和转录激活因子-1（STAT-1）的表达水平，并减少了白细胞介素-33（IL-33）的产生。ISTP和APE以剂量依赖性方式抑制胸腺和活化调节趋化因子（TARC/CCL17）的mRNA表达水平。蛋白质印迹分析表明，ISTP和APE剂量依赖性地抑制细胞间黏附分子-1的蛋白表达水平和STAT-1的磷酸化。本研究结果表明，ISTP可能通过STAT-1信号通路抑制人表皮角质形成细胞中TARC/CCL17的产生，并且可能与抑制IL-33的产生有关。当前研究表明，ISTP是APE中的一种活性成分，可能是治疗炎症性皮肤病的潜在治疗药物。
