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作 者:金双[1] 高连印[1] 赵梦培 车念聪[1] 张秋云[1] 杜宇琼[1]
机构地区:[1]首都医科大学中医药学院中医临床基础学系中医络病研究北京市重点实验室,北京100069
出 处:《首都医科大学学报》2018年第1期79-83,共5页Journal of Capital Medical University
基 金:北京市自然科学基金(7142023);北京市教委首都中医药研究专项(16ZY01)~~
摘 要:目的观察清毒汤对实验性重症肝损伤大鼠Bax、Bcl-2蛋白的表达以及肝细胞凋亡的影响,探讨该方对慢性重型肝炎(chronic severe hepatitis,CSH)大鼠肝细胞凋亡作用机制。方法建立硫代乙酰胺(thioacetamide,TAA)致实验性大鼠重症肝损伤模型,给予清毒汤干预后,用原位细胞凋亡技术法检测大鼠肝细胞凋亡指数(apoptotic index,AI)、蛋白免疫印迹法检测大鼠肝组织中Bax、Bcl-2蛋白表达的水平。结果与正常组比较,模型组AI显著增高(P<0.05),清毒汤各组较模型组AI明显降低,(P<0.01或P<0.05)。清毒汤对实验性肝损伤大鼠模型Bax蛋白表达具有抑制作用(P<0.01),对Bcl-2蛋白表达具有促进作用(P<0.01),能够提高Bcl-2/Bax的比值(P<0.01)。结论清毒汤可以调控Bax、Bcl-2蛋白表达量、降低AI,减轻肝细胞的凋亡和坏死。Objective To observe the effects of Qingdu decoction on the protein expressions of Bax,Bcl-2 and the apoptosis of liver cells in rats with severe liver injury and explore the mechanism of Qingdu decoction on treating hepatocyte apoptosis of the chronic severe hepatitis. Methods The severe liver injury rat model was induced by thioacetamide( TAA),and treated with Qingdu decoction. And then the hepatocyte apoptotic index( AI) was determined by terminal deoxynucleotidyl transferase-mediated d UTP nick end labeling( TUNEL)assay and the protein level of Bax,Bcl-2 in hepatic tissue was detected by Western blotting. Results The AI in model group was significantly increased when compared to that of in normal group( P〈0. 05). Compared to the model group,the AI was decreased significantly in each group of Qingdu decoction( P〈0. 01 or P〈0. 05). To the severe liver injury rat model,Qingdu decoction can cause the inhibition of the protein expressions of Bax( P〈0. 01),and dramatically increase the protein expressions of Bcl-2( P〈0. 01).Conclusion Qingdu decoction can regulate the protein expression level of Bax and Bcl-2,decrease AI,alleviate the degree of liver injury and apoptosis.
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