葡激酶对非酒精性脂肪性肝病大鼠的治疗作用观察

Therapeutic effect of staphylokinase on non-alcoholic fatty liver disease in rat model

目的探讨葡激酶对高脂饲料喂养所致大鼠脂肪肝的治疗作用。方法Wistar大鼠36只,随机均分为正常喂养(NC)组、高脂喂养模型(FL)组、高脂喂养治疗(TFL)组。后两组采用高脂饲料喂养法建立非酒精性脂肪性肝病(NAFLD)大鼠模型,TFL组在高脂饲养90d后,在继续高脂饲养的同时隔天尾静脉注射葡激酶0.5mg/kg,20d后处死大鼠。测定各组血清甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL)、丙二醛(MDA)、丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)水平;计算肝脏指数(肝湿重/体重),测定肝组织过氧化物酶增殖体激活受体α(PPAR-α)mRNA表达情况并行组织病理学检查。结果FL组肝脏指数(3.77±0.27)明显高于TFL组(3.48±0.29,P<0.05)和NC组(2.57±0.14,P<0.01),TFL组明显高于NC组(P<0.01)。与NC组比较,FL组大鼠血清TG、TC、LDL、AST水平明显升高(P<0.05或P<0.01),肝组织PPAR-αmRNA表达明显减少(P<0.01)。与FL组比较,TFL组大鼠血清TG、TC、LDL、MDA、AST水平明显降低P<0.05或P<0.01,肝组织PPAR-αmRNA表达明显增加(P<0.05)。TFL组肝脏指数为3.48±0.29,明显高于FL组(3.77±0.27,P<0.05)和NC组(2.57±0.14,P<0.01),FL组明显高于NC组(P<0.01)。结论葡激酶能够缓解高脂饲养大鼠的脂肪肝症状,其作用机制可能与上调肝脏PPAR-α基因表达水平有关。

Objective To observe the effects of staphylokinase （SAK） against non-alcoholic fatty liver disease in rats. Methods Sixteen Wistar rats were randomly divided into two groups, using high fat diet to set up non-alcoholic fatty liver disease model. Thirty six same strain rats were randomly divided into three groups： normal control group （NC）, fatty liver group （FL） and treated fatty liver groul5 （TFL）. After exposure to high fat diet 90 days, the treated fatty liver group was injected with SAK through vein. Changes of hepatic PPAR-α mRNA expression, pathology, and the serum ALT, AST, TG, TC, MDA, LDL and HDL in different groups were detected respectively. Results The serum AST, TG, TC, LDL in rats with high fat diet were markedly higher than that of rats fed with normal chow, while expression of PPAR-α mRNA decreased. The result indicated that non-alcoholic fatty liver disease model can be successful induced by high fat diet. Compared with FL group, the serum AST, TG, TC, LDL, MDA in the TFL group were markedly lower, while the expression of PPAR-a mRNA was increased. Conclusion Staphylokinase ameliorates the degree of Non-alcoholic fatty liver disease in rat model, the mechanisms of treating Non-alcoholic fatty liver disease may be related to promoting expression of PPAR-α.