中文摘要：

目的观察吲哚-3-原醇（I3C）对复合因素诱导肝纤维化大鼠的治疗作用并探讨其可能机制。方法采用复合因素（CCl4、酒精、高脂低蛋白饲料）制备大鼠肝纤维化模型,用I3C治疗10 d后,检测大鼠肝组织的羟脯氨酸（Hyp）、超氧化物歧化酶（SOD）、丙二醛（MDA）的含量;通过HE及Mas-son三色染色,观察肝脏病理学改变及胶原含量改变;免疫组化法观察肝脏中α-平滑肌肌动蛋白（α-SMA）的表达;West-ern blot检测肝组织中基质金属蛋白-2（MMP-2）的表达。结果与模型对照组比较,I3C治疗组肝组织Hyp含量降低,SOD活性升高,以大剂量（12 mg.kg-1）组明显（P〈0.01）,MMP-2蛋白表达升高;病理学改变尤其是胶原纤维的沉积明显减轻（P〈0.05）,α-SMA表达也降低。结论 I3C可促进复合因素所致大鼠肝纤维化模型的恢复,其机制与降低肝组织氧化应激、减少活化HSC数量以及促进基质胶原降解有关。

英文摘要：

Aim To investigate the effects of indole-3-carbinol（I3C） on multiple hepatotoxic factors-induced liver fibrosis in rats and its possible mechanism.Methods Male Wistar rats were divided randomly into six groups,a normal control group,a model control group,a I3C control group and fibrotic groups treated with three different doses of I3C.The fibrotic model was induced by multiple hepatotoxic factors,including carbon tetrachloride,ethanol and high fat/low proteins for 4 weeks.After completing models,rats in treatment groups were administered I3C 3,6 and 12 mg·kg-1 through intraperitoneal injection,daily for 10 days.Hepatic activity of superoxide dismutase（SOD）,he-patic malondialdehyde（MDA）and hepatic hydroxy proline（Hyp）content were determined.The liver his-tology and immunohistochemistry withα-smooth muscle actin（α-SMA）were assayed.Meanwhile,the expres-sion of matrix metalloproteinases-2（MMP-2）in liver was analyzed by Western blot.Results Compared with the fibrosis control group,hepatic content of Hyp was decreased by I3C treatment,and the activity of he-patic SOD was increased,especially in groups with I3C at the dose of 12 mg·kg-1（P0.01）.In addition,histopathological changes,especially changes of myofi-broblast proliferation,were reduced remarkably（P0.05）and the expression ofα-SMA was downregulated in the I3C-treated groups.As compared with fibrosis control group,the expression of MMP-2 was increased by I3C treatment.Conclusion I3C can promote the recovery of liver fibrosis in vivo.The mechanism might be due to protective effect for hepatocytes,reduction of the number of activated HSC and acceleration of colla-gen degradation.