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Salidroside ameliorates autophagy and activation of hepatic stellate cells in mice via NF-κB and TGF-β1/Smad3 pathways

Authors Feng J, Chen K, Xia Y, Wu L, Li J, Li S, Wang W, Lu X, Liu T, Guo C

Received 18 January 2018

Accepted for publication 3 April 2018

Published 22 June 2018 Volume 2018:12 Pages 1837—1853


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Sukesh Voruganti

Jiao Feng, Kan Chen, Yujing Xia, Liwei Wu, Jingjing Li, Sainan Li, Wenwen Wang, Xiya Lu, Tong Liu, Chuanyong Guo

Department of Gastroenterology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai, China

Purpose: 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.
Materials and methods: 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.
Results: 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.
Conclusion: Salidroside can effectively attenuate liver fibrosis by inhibiting the activation of HSCs in mice.

Keywords: liver fibrosis, salidroside, hepatic stellate cells, autophagy, TGF-β1/Smad3

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