辛伐他汀下调OX—LDL诱导的NRK52E细胞LOX-1表达和ROS生成

目的 探讨辛伐他汀对氧化低密度脂蛋白（ox-LDL）诱导的NRK52E细胞血凝素样氧化低密度脂蛋白受体（lectin-like ox-LDL receptor,LOX-1）表达和活性氧生成的作用.方法 体外培养NRK-52E,同步化后分为三组：（1）空白对照组（NRK52E细胞＋0μg/ml ox-LDL）；（2） ox-LDL组（NRK52E细胞＋50 μg/ml ox-LDL）；（3）辛伐他汀组（NRK52E细胞＋10μmol/L辛伐他汀＋50 μg/mlox-LDL）,用Western blot测定LOX-1蛋白表达,激光共聚焦检测ROS的表达.结果 （1）正常NRK52E细胞表达LOX-1非常低,50 μg/ml ox-LDL明显刺激NRK52E细胞表达LOX-1增加6.80倍,加用10 μmol/L辛伐他汀后,ox-LDL刺激的NRK52E细胞LOX-1表达降低65％；（2）正常NRK52E细胞内ROS生成很少,50 μg/ml ox-LDL可明显刺激NRK52E细胞内ROS生成增多了4.86倍,加用10μmol/L辛伐他汀后,ox-LDL刺激的NRK52E细胞ROS生成减少60％.结论 辛伐他汀可下调ox-LDL诱导的NRK52E细胞LOX-1表达和ROS生成,从而保护肾脏.

Simvastatin down regulation LOX-1 and ROS in NRK52E Induced by Ox-LDL

Objective To investigate the effect of Simvastatin on LOX-1 and ROS in NRK52E induced by ox-LDL.Methods NRK-52E cells were divided into three groups: Control group,ox-LDL group (50 μg/ml ox-LDL) and Simvastatin group (10 μmol/L Simvastatin +50 μg/ml ox-LDL).After incubation for 24 h,the expression of LOX-I was analyzed by Western blotting,and production of reactive oxygen species (ROS) was analyzed with confocal laser scanning microscopy.Results NRK-52E expressed LOX-1 at low level,50 μg/ml ox-LDL increased the expression of LOX-1 by 6.80 times.Pre - treatment with Simvastatin decreased LOX-1 expression by 65％.There was little ROS generation in NRK52E cells,50μg/ml ox-LDL promoted the expression of LOX-1 by 4.86.times.Pre - treatment with Simvastatin decreased ROS generation by 60％.Conclusions Simvastatin upregulate LOX-1 expression and ROS generation induced by Ox-LDL in NRK52E cells.