BACKGROUND: 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. OBJECTIVE: 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. METHODS: 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)-α levels were measured. RESULTS: Captopril treatment decreased the hepatic content of the proinflammatory cytokine TNF-α and increased the anti-inflammatory cytokine IL-10. CONCLUSION: the present study suggests that the protective effect of captopril on hepatic fibrosis is likely to be mediated by cytokine production.
BACKGROUND: 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. OBJECTIVE: 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. METHODS: 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)-α levels were measured. RESULTS:Captopril treatment decreased the hepatic content of the proinflammatory cytokine TNF-α and increased the anti-inflammatory cytokine IL-10. CONCLUSION: the present study suggests that the protective effect of captopril on hepatic fibrosis is likely to be mediated by cytokine production.