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Inhibitory effect of angiotensinⅡreceptor antagonist on hepatic stellate cell activation in non-alcoholic steatohepatitis 被引量:10

Inhibitory effect of angiotensinⅡreceptor antagonist on hepatic stellate cell activation in non-alcoholic steatohepatitis
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摘要 AIM: To investigate the efficacy of angiotensin Ⅱ receptor antagonist on hepatic stellate cells (HSCs) activation in the patients with non-alcoholic steatohepatitis (NASH). METHODS: Seven patients with NASH were prescribed Iosartan, a selective angiotensin Ⅱ type 1 receptor antagonist (50 mg/d) for 48 wk. Liver biopsies were performed both at the entry and end of the study in all patients. Quiescent and activated HSCs were identified by double immunostaining using anti-p75 and α-smooth muscle actin antibodies, and the number of each phenotype was counted. Similarly, the liver specimens obtained from the eight patients with non-alcoholic fatty liver (NAFL) were also examined as controls. RESULTS: In NASH hepatic tissues, activated HSCs were dominantly distributed as compared with those in NAFL. The 48-wk Iosartan treatment induced a remarkable decrease in activated HSCs and a mild increase in quiescent phenotypes. CONCLUSION: Our data suggest the crucial involvement of HSCs in anti-fibrotic effect of angiotensin Ⅱ receptor antagonist on patients with NASH. AIM: To investigate the efficacy of angiotensinⅡreceptor antagonist on hepatic stellate cells (HSCs) activation in the patients with non-alcoholic steatohepatitis (NASH). METHODS: Seven patients with NASH were prescribed losartan, a selective angiotensinⅡtype 1 receptor antagonist (50 mg/d) for 48 wk. Liver biopsies were performed both at the entry and end of the study in all patients. Quiescent and activated HSCs were identified by double immunostaining using anti-p75 andα-smooth muscle actin antibodies, and the number of each phenotype was counted. Similarly, the liver specimens obtained from the eight patients with non-alcoholic fatty liver (NAFL) were also examined as controls. RESULTS: In NASH hepatic tissues, activated HSCs were dominantly distributed as compared with those in NAFL. The 48-wk losartan treatment induced a remarkable decrease in activated HSCs and a mild increase in quiescent phenotypes. CONCLUSION: Our data suggest the crucial involvement of HSCs in anti-fibrotic effect of angiotensinⅡreceptor antagonist on patients with NASH.
出处 《World Journal of Gastroenterology》 SCIE CAS CSCD 2006年第2期322-326,共5页 世界胃肠病学杂志(英文版)
基金 Supported by a Grant-in-Aid for Scientific Research (C) from the Japan Society for the Promotion of Science, No. 15590613,and a grant for Research on Intractable Disease from the Japanese Ministry of Public Welfare
关键词 NASH NAFLD Hepatic fibrosis HSC LOSARTAN NASH NAFLD 肝纤维化 HSC 血管紧张素
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  • 1Haruki Senoo.Structure and function of hepatic stellate cells[J].Medical Electron Microscopy.2004(1)

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