Amirshahrokhi Keyvan, Ghazi-khansari Mahmoud, Mohammadi-Farani Ahmad, Karimian Golnar
Department of Pharmacology, School of Medicine, Ardebil University of Medical Sciences, Ardebil, Iran.
Iran J Immunol. 2010 Dec;7(4):247-51.
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)-α levels were measured.
Captopril treatment decreased the hepatic content of the proinflammatory cytokine TNF-α 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.
肾素-血管紧张素系统在肝脏炎症和纤维化中起重要作用。血管紧张素转换酶（ACE）抑制剂阻断肾素-血管紧张素系统可对肝纤维化产生一定的保护作用。卡托普利作为一种ACE抑制剂，可减少炎症介质并减轻胆管结扎（BDL）大鼠肝脏的肝纤维化。
本研究旨在探讨卡托普利对大鼠胆管结扎模型诱导的肝纤维化中细胞因子产生的影响。
雄性大鼠分为四组，包括对照组、假手术组、BDL组和BDL加卡托普利组（10mg/kg/天，口服）。治疗28天后，取出肝脏进行细胞因子分析。检测肝脏白细胞介素（IL）-10和肿瘤坏死因子（TNF）-α水平。
卡托普利治疗降低了促炎细胞因子TNF-α的肝脏含量，并增加了抗炎细胞因子IL-10。
本研究表明，卡托普利对肝纤维化的保护作用可能是由细胞因子产生介导的。
