【摘要】 目的:研究黄芪甲苷的抗肝损伤作用机制。方法:雄性C57鼠采用腹腔注射CCl₄构建肝损伤模型,同时采用黄芪甲苷（20 mg/kg、40 mg/kg）和阳性药扶正化瘀胶囊（750 mg/kg）进行灌胃,HE染色检测肝损伤的变化;生化检测血清丙氨酸转移酶（ALT）和天冬氨酸转移酶（AST）、超氧化歧化酶（SOD）、丙二醛（MDA）;采用ELISA检测血清中的白介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）;Western blot法检测肝脏中TGF-β及Smad-3的蛋白表达。结果:黄芪甲苷（20 mg/kg、40 mg/kg）组和扶正化瘀胶囊（750mg/kg）组显著抑制CCl₄诱导的小鼠肝损伤程度,与纤维化模型组相比,黄芪甲苷（20 mg/kg、40 mg/kg）组和扶正化瘀胶囊（750 mg/kg）组血清ALT、AST水平及MDA水平明显降低及IL-6、TNF-α,SOD显著提高;黄芪甲苷（20 mg/kg、40 mg/kg）组和扶正化瘀胶囊（750 mg/kg）组显著抑制肝组织中TGF-β和smad-3的蛋白表达。结论:黄芪甲苷具有显著的改善肝损伤作用。更多还原

【Abstract】 Objective: To investigate the anti-hepatofibrotic effects of astragaloside IV（ AS） on liver fibrosis. Methods: Male C57 mice were induced with 20% CCl₄（ 2ml/kg） for 6weeks to induce liver fibrosis,and were treated with intragastrical gavage of 20 and 40 mg/kg AS for14 d since the fifth week of CCl₄ induction. Liver fibrosis of the mice was evaluated by HE stain. Activities of serum alanine aminotransferase（ ALT） and aspartate aminotransferase（ AST）,and serum content of SOD and MDA were measured with automated biochemistry analyzer.The protein levels of transforming growth factor beta（ TGF-β） and Smad-3 were detected by Western blot analysis. Results : AS（ 20 mg / kg,40 mg / kg） groups significantly attenuates the progression of liver fibrosis induced by CCl₄. Treatment with AS（ 20 mg / kg,40 mg / kg）groups also resulted in significant decreases in the serum levels of ALT and AST,as well as the content of MDA and increased SOD. AS（ 20 mg / kg,40 mg / kg） groups significantly reduced the protein expression levels of TGF-β and Smad-3 in the liver. AS exerts anti-fibrotic effects on the liver induced by CCl₄.更多还原