目的：观察2型糖尿病大鼠氧化型低密度脂蛋白受体-1（LOX-1)、内皮型一氧化氮合酶（eNOS)、过氧化物酶体增殖物激活受体γ（ PPARγ)在肝脏的表达以及罗格列酮对其表达的影响。方法选择雄性Wistar大鼠80只，随机分为对照（空白对照)组、高脂组、糖尿病组、罗格列酮组，每组20只。对照组用普通饲料喂养，另3组用高脂饲料喂养，对糖尿病组和罗格列酮组制备2型糖尿病大鼠模型，造模成功后罗格列酮组予罗格列酮4 mg/（ kg·d)灌胃。造模成功后6周和12周时，留取各组动物肝脏组织检测LOX-1、eNOS、PPARγ的蛋白表达。结果①LOX-1表达：造模成功后6周和12周时，与对照组和高脂组比较，糖尿病组表达上调（ P0．05)；造模成功后12周时罗格列酮组较糖尿病组表达上调（P<0．01)。③PPARγ表达：造模成功后6周和12周时，与对照组比较，高脂组、糖尿病组和罗格列酮组表达上调（P<0．01)；与高脂组比较，糖尿病组和罗格列酮组表达上调（P<0．01)；罗格列酮组较糖尿病组表达下调（P<0．01)。结论高血糖、高血脂均可导致大鼠肝脏LOX-1、eNOS和PPARγ的表达异常，且高血糖和高血脂并存时表达异常更明显。罗格列酮对这种表达的异常有一定逆转作用。%Objective To study the protein expression of LOX-1, eNOS and PPARγin livers in type 2 diabetes rats, and to study the intervention effect of rosiglitazone. Methods A total of 80 male Wistar rats were randomized to control group, high fat diet group, diabetes group, and Rosiglitazone treatment group. With 20 rats in each group. The rats in the control group were fed with normal diet, the other 3 groups were fed with high fat diet, type 2 diabetes models were developed in diabetes group and Rosiglitazone group. Rosiglitazone group was treated with Rosiglitazone. After treatment with Rosiglita-zone for 6 weeks and 12 weeks, the rats were sacrificed. Liver tissues were collected for protein expression of LOX-1, eNOS, PPARγ. Results ① Expression of LOX-1:Compared with control group and Rosiglitazone group, the liver protein expres-sion of LOX-1 in diabetes group was up-regulated 6 weeks after the model was established(P<0. 01). And compared with di-abetes group, the expression of LOX-1 in Rosiglitazone group was down-regulated 6 weeks after the model was established (P<0. 01). Compared with control group, the expressions of LOX-1 in high fat diet group, diabetes group and Rosiglitazone group were up-regulated 12 weeks after the model was established(P<0. 01). The expression of LOX-1 in diabetes group and Rosiglitazone group were up-regulated compared with those in high fat diet group 12 weeks after the model was established (P<0. 01). The expression of LOX-1 in Rosiglitazone group was down-regulated compared with those in diabetes group 12 weeks after the model was established(P<0. 01). ②Expression of eNOS:Compared with control group, the liver protein ex-pression of eNOS in high fat diet group, diabetes group and Rosiglitazone group were down-regulated 6 weeks and 12 weeks af-ter the model was established(P<0. 01). And compared with high fat diet group, the expressions of eNOS in diabetes group and Rosiglitazone group were down-regulated 6 weeks and 12 weeks after the model was established(P<0. 01). The expres-sion of eNOS in Rosiglitazone group was up-regulated compared with that of diabetes group 12 weeks after the model was estab-lished (P<0. 01). ③Expressions of PPARγ:6 weeks and 12 weeks after the model was established, compared with control group, the liver protein expressions of PPARγin high fat diet group, diabetes group and Rosiglitazone group were up-regulated (P<0. 01). And the expressions of PPARγ in diabetes group and Rosiglitazone group were up regulated more than that of high fat diet group(P<0. 01). The expression of PPARγin Rosiglitazone group was down-regulated more than that of diabetes group(P<0. 01). Conclusion Both hyperglycemia and hyperlipidemia can induce abnormal protein expression of LOX-1, eNOS and PPARγ in liver. When hyperglycemia coexists with hyperlipidemia, the abnormal expression is more obvious and thiazolidinediones Rosiglitazone drug has some reversing function in the abnormal expression.
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