辛伐他汀保护高脂血症肾损害大鼠机制探讨

Investigation of mechanism of Simvastatin in protecting lipid-renal damage rats

目的探讨辛伐他汀对高脂血症大鼠肾损害的保护机制。方法实验包括正常对照组、高脂血症模型组和辛伐他汀10mg/(kg.d)治疗组,12周后检测三组大鼠的血脂变化及观察尿蛋白水平,外周血及肾皮质NO浓度。结果高脂血症组尿蛋白明显高于正常对照组,血清及肾组织NO水平低于正常对照组。辛伐他汀治疗组总胆固醇(TC)、甘油三脂(TG)、低密度脂蛋白胆固醇(LDL-C)显著低于高脂血症组,且尿蛋白也显著低于高脂血症组,血清及肾组织NO含量高于高脂血症组。结论辛伐他汀在调脂的同时,促进NO的生成,降低尿蛋白。NO的增加可能是辛伐他汀保护高脂血症肾损害的重要机制之一。

[Objective] To study the mechanism of Simvastatin in protecting lipid-renal damage rats by investigating simvastatin on the serum levels of lipid, Cr, urine protein and NO content in serum and renal cortex. [Methods] Thirty rats were randomly divided into 3 groups： control group, hyperlipidemic group （HL-untreated） and Gemfibrozil-treated group （HL-treated, 10 mg（kg.d）. The serum levels of lipid, Cr, urine protein and NO content in serum and renal cortex were measured. [Results] Hyperlipidemic rats had higher level of urine protein and lower level of NO in serum and renal cortex compared with those of control subjects. Significant decrease of level of urine protein and serum lipid and increase of NO in serum and renal cortex were found in Simvastatin-treated rats. [Conclusions] Simvastatin can regulate dyslipidemia, increase the NO content and decrease urine protein. Simvastatin can restore endothelial function and inhibit atherogenesis. Increasing of NO may be ones of the most mechanism of Gemtibrozil in protecting lipid-renal damage.