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CCl_4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CCl_4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。
Objective: To investigate the anti-hepatofibrotic effects of astragaloside IV (AS) on liver fibrosis. Methods: Male C57 mice were in- duced with 20% CC14 (2ml/kg) for 6weeks to induce liver fibrosis, and were treated with intragastrical garage of 20 and 40 mg/kg AS forl4d since the fifth week of CC14 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 CC14. 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-I3 and Smad-3 in the liver. AS exerts anti-fibrotic effects on the liver induced by CC14.
出处
《中药药理与临床》
CAS
CSCD
北大核心
2015年第6期24-27,共4页
Pharmacology and Clinics of Chinese Materia Medica
基金
黑龙江中医药大学优秀创新人才支持计划(项目编号:2012RCQ62)