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World J Gastroenterol. Feb 21, 2014; 20(7): 1822-1832
Published online Feb 21, 2014. doi: 10.3748/wjg.v20.i7.1822
Published online Feb 21, 2014. doi: 10.3748/wjg.v20.i7.1822
Sophocarpine attenuates liver fibrosis by inhibiting the TLR4 signaling pathway in rats
Hui Qian, Jian Shi, Ting-Ting Fan, Si-Wen Chen, Chun-Yan Song, Wei-Fen Xie, Yue-Xiang Chen, Department of Gastroenterology, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai 200003, China
Hui Qian, Jiao Lv, Zhi-Wu Zheng, Department of Gastroenterology, the 411th Hospital of PLA, Shanghai 200081, China
Author contributions: Qian H, Shi J and Fan TT contributed equally to this study who performed the majority of the experiments and prepared the manuscript with assistance from Chen SW and Song CY; Lv J and Zheng ZW performed the immunohistochemical staining and data analysis; Xie WF designed the experiments and supervised the project; Chen YX designed the experiments, analyzed the data and wrote the manuscript.
Supported by The National Natural Science Foundation of China, Nos. 30971343, 81270486, 81000167 and 81370009
Correspondence to: Yue-Xiang Chen, Professor, Department of Gastroenterology, Shanghai Changzheng Hospital, Second Military Medical University, 415 Fengyang Rd, Shanghai 200003, China. yuexchen1807@163.com
Telephone: +86-21-81885343 Fax: +86-21-81886824
Received: September 7, 2013
Revised: November 13, 2013
Accepted: November 28, 2013
Published online: February 21, 2014
Revised: November 13, 2013
Accepted: November 28, 2013
Published online: February 21, 2014
Core Tip
Core tip: Sophocarpine significantly ameliorated liver function and hepatic fibrosis in both the dimethylnitrosamine and bile duct ligation models. In addition, sophocarpine inhibited the activation and proliferation of hepatic stellate cells in vitro, which contributed to the anti-fibrotic effect of sophocarpine in vivo. Toll-like receptor 4 signaling was blocked by sophocarpine in vivo and in vitro, accompanied by a reduction in pro-inflammatory and fibrotic cytokines, as well a decrease in the expression of Cyclin D1 and proliferating cell nuclear antigen.