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目的:探讨茵陈色原酮对小鼠急性乙醇性肝损伤的保护作用及其机制。方法:实验小鼠随机分为5组:模型组、茵陈色原酮(高、中、低剂量)组和正常对照组,每组各6只。给予茵陈色原酮组小鼠相应剂量的茵陈色原酮灌胃7d,第7天时将模型组、茵陈色原酮组小鼠采用50%乙醇12mL/(kg·d)灌胃,禁食12h,致小鼠急性乙醇性肝损伤;观察小鼠肝脏组织形态,计算肝脏指数(LI),ELISA法测定小鼠血清丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)、总蛋白(TP)、肝胞浆乙醛脱氢酶(ALDH)、谷胱甘肽过氧化物酶(GSH-Px)水平。结果:茵陈色原酮(高、中剂量)组均明显降低急性乙醇性肝损伤小鼠肝脏指数(P<0.01);高剂量组可减轻肝组织脂肪变性(P<0.05),明显降低血清ALT、AST水平(P<0.01),升高肝胞浆ALDH、GSH-Px水平(P<0.01)与血清TP水平(P<0.01)。结论:茵陈色原酮对小鼠急性乙醇性肝损伤具有保护作用,其机制与增强肝脏清除乙醛和抗氧化能力有关。
Objective: To investigate the protective effect and mechanism of injection of PRA on acute ethanol-induced liver injury in mice. Methods: The experimental mice were randomly divided into 5 groups: model group, Yinchuan chromogen (high, medium and low dose) group and normal control group, 6 in each group. At the 7th day, mice in the model group and Yinchuan chromogenic ketone group were treated with 50% ethanol 12mL / (kg · d) Fasting alcoholic liver injury was induced in mice for 12h, the liver morphology of mice was observed and the liver index (LI) was calculated. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) Total protein (TP), hepatic cytoplasmic ALDH, and glutathione peroxidase (GSH-Px). (P <0.01). The high dose group could reduce the fatty degeneration of liver tissue (P <0.05) and significantly reduce the serum level of hepatic steatosis ALT and AST (P <0.01), and increased ALDH, GSH-Px levels (P <0.01) and serum TP levels (P <0.01). CONCLUSION: PRA has a protective effect on acute ethanol-induced liver injury in mice, and its mechanism is related to the enhancement of hepatic clearance of acetaldehyde and antioxidation.