Astilbin inhibits Th17 cell differentiation and ameliorates imiquimod-induced psoriasis-like skin lesions in BALB/c mice via Jak3/Stat3 signaling pathway
Astilbin inhibits Th17 cell differentiation and ameliorates imiquimod-induced psoriasis-like skin lesions in BALB/c mice via Jak3/Stat3 signaling pathway
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Astilbin 通过 Jak3/Stat3 信号通路抑制 Th17 细胞分化并改善 BALB/c 小鼠中咪喹莫特诱导的银屑病样皮肤病变
DOI:
10.1016/j.intimp.2015.12.035
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发表时间:
2016-03-01
影响因子:
5.6
通讯作者:
Li, Ping
中科院分区:
文献类型:
--
作者:
Di, Ting-Ting;Ruan, Zhi-Tong;Li, Ping
The flavonoid astilbin is the major active component extracted from the rhizome of Smilax glabra, which has been widely used in China to treat inflammatory and autoimmune diseases, Psoriasis is a common chronic inflammatory disease in which T helper 17 (Th17) cells play an important role, provoking inflammation. We employed an imiquimod (IMQ)-induced psoriasis-like mouse model to investigate the effect of astilbin in inflammation. Mice were administered 25 to 50 mg/kg astilbin. Inflammation of psoriasis-like lesions was assessed by histology, circulating levels of T cells were assessed by flow cytometry and cytoldnes by bead-based immunoassay. Jak/Stat3 in isolated T cells was assessed by Western blotting and ROR gamma t expression was assessed by RT-PCR Administration of astilbin ameliorated IMQ-induced keratinocyte proliferation, infiltration of CD3+ cells to psoriatic lesions and ameliorated elevations in circulating CD4+ and CD8+ T cells and inflammatory cytokines (IL-17A, TNF-alpha, IL-6, IFN-gamma and IL-2). In vitro, astilbin inhibited Th17 cell differentiation and IL-17 secretion of isolated T cells, and inhibited Jak/Stat3 signaling in Th17 cells, while up-regulating Stat3 inhibitor SCOSE3 expression in psoriatic lesions. Thus, astilbin likely alleviates psoriasis-like skin lesions by inhibiting Th17 related inflammation. Astilbin represents as an interesting candidate drug for immunoregulation of psoriasis. (C) 2016 The Authors. Published by Elsevier B.V.