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IJI-Iranian Journal of Immunology. 2010; 7 (4): 247-251
in English | IMEMR | ID: emr-104252

ABSTRACT

The renin-angiotensin system has an important role in hepatic inflammation and fibrosis. Renin-angiotensin system blockade by angiotensin-converting enzyme [ACE] inhibitors provides some protective effects against hepatic fibrogenesis. Captopril as an ACE inhibitor can decrease inflammatory mediators and attenuate hepatic fibrosis in the livers of bile duct ligated [BDL] rats. The present study was conducted to investigate the effects of captopril on cytokine production in hepatic fibrosis induced by a bile duct ligation model in rats. Male rats were divided into four groups including; control, sham operated, BDL, and BDL plus captopril [10 mg/kg/day, orally]. After 28 days of treatment, the livers were removed for cytokine analysis. Hepatic interleukin [IL]-10 and tumor necrosis factor [TNF]- alpha levels were measured. Captopril treatment decreased the hepatic content of the proinflammatory cytokine TNF- alpha and increased the anti-inflammatory cytokine IL-10. The present study suggests that the protective effect of captopril on hepatic fibrosis is likely to be mediated by cytokine production

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