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目的探讨硫普罗宁对实验性梗阻性黄疸大鼠肝功能的保护作用及作用机理。方法SD大鼠胆总管结扎后分2组,每组20只,分别用1m l硫普罗宁或生理盐水腹腔注射。假手术组20只。分别于术后10d、20d(每小组n=10)心脏取血测定血清超氧化物歧化酶(SOD)、丙二醛(MDA)含量,同时测定谷丙转氨酶(AST)、直接胆红素(DB)和总胆汁酸(TBA)浓度,并对肝脏行光镜下病理形态学观察。结果血清MDA浓度在梗阻10d即升高,且随胆道梗阻时间延长进一步升高,SOD在梗阻10d后即下降,同时伴有血清AST、DB和TBA的升高和肝脏病理形态学的进行性改变。硫普罗宁治疗组MDA显著低于对照组而SOD显著高于对照组,并能改善肝组织病理形态。结论大鼠梗阻性黄疸时,氧自由基损害可能是肝损伤的原因,硫普罗宁通过抗氧化作用对梗阻性黄疸大鼠的肝脏起保护作用。
Objective To investigate the protective effect and mechanism of tiopronin on liver function in experimental obstructive jaundice rats. Methods The common bile duct of SD rats was divided into 2 groups (20 rats in each group), which were injected intraperitoneally with 1 ml of tiopronin or normal saline respectively. 20 sham operation group. Serum levels of SOD and MDA were measured at 10 and 20 days after operation respectively (n = 10 in each group). Serum levels of alanine aminotransferase (AST) and direct bilirubin DB) and total bile acid (TBA) were measured. Pathological changes of liver were observed under light microscope. Results The level of serum MDA increased at the 10th day after obstruction and further increased with the prolongation of biliary obstruction. The SOD decreased at the 10th day after obstruction, accompanied by the increase of serum AST, DB and TBA and the progressive change of liver pathomorphology . SOD in the tiopronin treatment group was significantly lower than that in the control group, and SOD was significantly higher than that in the control group, and liver tissue pathology was also improved. Conclusion Oxygen free radical damage may be the cause of liver injury in rats with obstructive jaundice. Tiopronin may play a protective role in the liver of rats with obstructive jaundice through antioxidation.