Telmisartan prevents hepatic fibrosis and enzyme-altered lesions in liver cirrhosis rat induced by a choline-deficient L-amino acid-defined diet |
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Authors: | Jin Haiyan Yamamoto Naoki Uchida Koichi Terai Shuji Sakaida Isao |
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Affiliation: | aDepartment of Gastroenterology and Hepatology, Yamaguchi University Graduate School of Medicine, Minami-Kogushi 1-1-1 Ube, Yamaguchi 755-8505, Japan;bDepartment of Gastroenterology and Hepatology, Yanbian University Hospital, Yanji, Jilin, China |
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Abstract: | Rennin-angiotensin system is involved in liver fibrogenesis through activating hepatic stellate cells (HSCs). Telmisartan (Tel) is an angiotensin II type 1 receptor antagonist, could function as a selective peroxisome proliferator-activated receptor γ activator. Here we studied the effect of Tel on liver fibrosis, pre-neoplastic lesions in vivo and primary HSCs in vitro. In vivo study, we used the choline-deficient l-amino acid-defined (CDAA)-diet induced rat NASH model. The rats were fed the CDAA diet for 8 weeks to induce liver fibrosis and pre-neoplastic lesions, and then co-administrated with Tel for another 10 weeks. Tel prevented liver fibrogenesis and pre-neoplastic lesions by down-regulating TGFβ1 and TIMP-1, 2 and increasing MMP-13 expression. Tel inhibited HSCs activation and proliferation. These results suggested that Tel could be a promising drug for NASH related liver fibrosis. |
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Keywords: | Angiotensin II type 1 receptor antagonist Fibrosis Hepatic stellate cell(s) Nonalcoholic steatohepatitis |
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