Salidroside ameliorates autophagy and activation of hepatic stellate cells in mice via NF-κB and TGF-β1/Smad3 pathways.
Salidroside ameliorates autophagy and activation of hepatic stellate cells in mice via NF-κB and TGF-β1/Smad3 pathways.
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红景天苷通过 NF-κ B 和 TGF-β 1/Smad3 途径改善小鼠肝星状细胞的自噬和激活
DOI：
10.2147/dddt.s162950
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发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Guo C
中科院分区：
文献类型：
--
作者：
Feng J;Chen K;Xia Y;Wu L;Li J;Li S;Wang W;Lu X;Liu T;Guo C
肝纤维化是慢性肝病的常见疾病和必经阶段。本研究旨在探讨红景天苷对小鼠肝纤维化的影响及其可能机制。采用四氯化碳(CCl4)腹腔注射8周和胆管结扎14天的方法建立小鼠肝纤维化模型。红景天苷10 mg/kg和20 mg/kg，1次/d。采用实时定量聚合酶链式反应、酶联免疫吸附试验、Western印迹、免疫组织化学和免疫荧光等方法检测基因和蛋白的表达水平。红景天苷抑制两种肝纤维化模型细胞外基质(ECM)的产生，调节MMP2/TIMP1的平衡，从而减轻肝纤维化。红景天苷通过核因子-βB信号通路减少枯否细胞和肝星状细胞产生转化生长因子-κ1，从而通过下调转化生长因子-β1/Smad3信号通路抑制肝星状细胞的激活和自噬。红景天苷可通过抑制小鼠肝星状细胞的活化而有效地减轻肝纤维化。
Liver fibrosis is commonly seen and a necessary stage in chronic liver disease. The aim of this study was to explore the effect of salidroside on liver fibrosis in mice and its potential mechanisms. Two mouse liver fibrosis models were established by intraperitoneal injection of carbon tetrachloride (CCl4) for 8 weeks and bile duct ligation for 14 days. Salidroside was injected intraperitoneally at doses of 10 and 20 mg/kg once a day. Gene and protein expression levels were determined by quantitative real-time polymerase chain reaction, enzyme-linked immunosorbent assay, Western blot, immunohistochemistry, and immunofluorescence. Salidroside inhibited the production of extracellular matrix (ECM) and regulated the balance between MMP2 and TIMP1 and, therefore, alleviated liver fibrosis in the two fibrosis models. Salidroside reduced the production of transforming growth factor (TGF)-β1 in Kupffer cells and hepatic stellate cells (HSCs) via the nuclear factor-κB signaling pathway and, therefore, inhibited the activation of HSCs and autophagy by downregulation of the TGF-β1/Smad3 signaling pathway. Salidroside can effectively attenuate liver fibrosis by inhibiting the activation of HSCs in mice.