辛伐他汀对糖尿病大鼠血脂和血小板膜糖蛋白表达水平的影响

Effect of simvastatin on the expression of platelet membrane glycoprotein in diabetic rats

目的探讨羟甲基戊二酸单酰辅酶A(HMG-CoA)还原酶抑制剂辛伐他汀对2型糖尿病大鼠血脂和血小板膜糖蛋白表达的影响。方法雌性Wistar大鼠腹腔注射链脲佐菌素(STZ)建立糖尿病模型,造模成功后将其随机分为糖尿病组、辛伐他汀组[辛伐他汀混悬液灌胃,20 mg/(kg·d),共用12周]各10只,另取10只健康大鼠设为对照组,12周后测定及比较各组血脂及血小板膜糖蛋白CD62p、CD63、CD61、CD41的表达。结果糖尿病组总胆固醇、甘油三酯和LDL水平高于对照组,而HDL的水平低于对照组(P<0.01);辛伐他汀组总胆固醇、甘油三酯和LDL水平低于糖尿病组,而HDL水平高于糖尿病组(P<0.01);糖尿病组血小板膜糖蛋白CD62p和CD63水平较对照组高(P<0.01),辛伐他汀组的CD62p和CD63水平较糖尿病组低(P<0.01);3组血小板膜糖蛋白CD61、CD41水平比较差异无统计学意义(P>0.05)。结论辛伐他汀能调节糖尿病大鼠的血脂水平,能降低血小板膜糖蛋白CD62p和CD63的水平,抑制血小板的聚集。

Objective To investigate the effect of simvastatin on serum lipids and the expression of platelet membrane glycoproteins in diabetic rats. Methods Type 2 diabetes model was established in female Wistar rats by intraperitoneal injection of streptozotocin. Diabetic rats were randomly divided into diabetic group （n=10）and simvastin group [n=10,received simvastatin gavaging for 12 weeks ,20 mg/（kg＆#183;d）],10 healthy normal rats were selected as control group. Flow cytometric analysis was applied to detect the expression of CD62p,CD63,CD61 and CD41 on the surface of platelet after 12 weeks of treatment.Result Compared with control group,the serum levels of total cholesterol （TC）,triglyceride （TG）and low density lipoprotein （LDL）were increased significantly in diabetic group but the serum level of high density lipoprotein （HDL） was decreased （P＆lt;0.01）. The serum levels of TC,TG and LDL in simvastin group were lower than those of diabetic group,but the level of HDL level was higher （P＆lt;0.01）. The expressions of CD62p and CD63 on the surface of platelet in diabetic group were higher than those of control group （P＆lt;0.01）,but simvastatin signifi-cantly decreased their expressions in diabetic rats （P＆lt;0.01）. However,there was no difference in the expres-sions of CD61 and CD41 among three groups. Conclusion Simvastatin can regulate serum lipids and decrease the expressions of CD62p and CD63 on the surface of platelet in diabetic rats,and then inhibit aggregation of platelet.