解偶联蛋白2在PM2.5所致氧化应激损伤心肌细胞中作用机制探讨.docVIP

解偶联蛋白2在PM2.5所致氧化应激损伤心肌细胞中作用机制探讨 　　【摘要】 目的：初步探讨解偶联蛋白2（UCP2）在PM2.5致心肌细胞氧化应激损伤中的作用。方法：培养大鼠心肌细胞株H9C2细胞，分为NC组、PM2.5组、PM2.5+siRNA组三组，分别给予常规的培养基、PM2.5培养基、siRNA+PM2.5培养基刺激，48 h后比色法检测线粒体的活性氧（ROS）、丙二醛（MDA）含量、谷胱甘肽（GSH）含量以及超氧化物歧化酶（SOD）活性。结果：PM2.5组心肌细胞内ROS、MDA含量、GSH含量、SOD活性分别为（69.2±6.3）U/Well、（68.33±1.96）nmol/mgprot、（533.05±10.83）mg/gprot、（50.37±1.98）U/mgprot，PM2.5+siRNA组心肌细胞内ROS（90.2±6.2）U/Well明显增多、MDA含量（88.44±1.27）nmol/mgprot明显升高，GSH含量（421.17±16.90mg/gprot）明显减少，SOD活性（30.09±2.02）U/mgprot明显降低。三组两两比较差异均有统计学意义（P0.05）。结论：PM2.5可以通过氧化应激途径损伤心肌细胞，RNA干扰UCP2基因表达后，PM2.5致氧化应激增强所介导的心肌细胞损伤加剧，这提示UCP2在PM2.5致氧化应激心肌损伤过程中可能起着保护性作用。 　　【关键词】 解偶联蛋白2； PM2.5； H9C2； 心肌细胞； 活性氧； 丙二醛； 谷胱甘肽； 超氧化物歧化酶 　　【Abstract】 Objective： To investigate the effect of UCP2 during the oxidative stress injury procedure of PM2.5 on the rat myocardial cells H9C2. Method： Rat cardiomyocytes H9C2 cell lines were cultured，and divided into 3 groups，the NC group was used of conventional medium stimulus，the PM2.5 group was used of PM2.5 medium stimulus and the PM2.5+siRNA group was used of PM2.5+siRNA medium stimulus. After 48 hours，the activity of reactive oxygen species （ROS） and superoxide dismutase （SOD）， and the content of malonaldehyde （MDA） and glutathione （GSH），were determinated by colorimetric detection.Result：The PM2.5 group of intracellular ROS，MDA， the content of GSH，and the activity of SOD，were respectively （69.2±6.3）U/Well，（68.33±1.96）nmol/mgprot，（533.05±10.83）mg/gprot，（50.37±1.98）U/mgprot.Compared with PM2.5 group，the PM2.5+siRNA group of intracellular ROS was （90.2±6.2）U/Well increased greatly，MDA was（88.44±1.27）nmol/mgprot increased greatly，the content of GSH was （421.17±16.90）mg/gprot and the activity of SOD was（30.09±2.02）U/mgprot. Compared the three groups，all the differences were statistically significant（P0.05）. Conclusion：PM2.5 can lead to myocardial cell damage by oxidative stress， and the silence of UCP2 by RNAi lead to aggravate the injury of H9C2 cells， indicating that UCP2 may play an protective effec