过氧化物酶体增殖物受体γ对血管内皮细胞活性氧生成的影响及机制  被引量:1

Effect and mechanism of PPARγon the generation of ROS in vascular endothelial cells

在线阅读下载全文

作  者:王兆君[1] 张宝和[1] 

机构地区:[1]中国人民解放军海军总医院干部保健科,北京100048

出  处:《检验医学与临床》2015年第24期3643-3644,3647,共3页Laboratory Medicine and Clinic

摘  要:目的分析过氧化酶体增殖物受体γ(PPARγ)在高糖介导血管内皮细胞活性氧(ROS)生成中的影响与机制。方法采用33.0mmol/L D-葡萄糖(高糖)进行介导的人脐静脉内皮细胞作为高糖介导组,采用二甲基亚砜处理的人脐静脉内皮细胞作为对照组。分别采用3种PPARγ激动剂吡格列酮、GW9662、京尼平作用于高糖介导组。采用一氧化氮与超氧阴离子荧光探针判定3种药物对血管内皮细胞一氧化氮与ROS的影响,采用蛋白免疫印迹法评估解耦联蛋白2表达水平。结果高糖介导组ROS与一氧化氮表达水平与对照组比较差异有统计学意义(P<0.05)。3种药物中,吡格列酮对血管内皮细胞ROS、一氧化氮与解耦联蛋白2的作用最强(P<0.05)。结论 PPARγ能够明显缓解高糖介导下血管内皮细胞ROS生成,主要通过上调解耦联蛋白2发挥作用。Objective To investigate the effect and mechanism of PPARγon the generation of reactive oxygen species(ROS)in vascular endothelial cells induced by high concentration glucose.Methods Human umbilical vein endothelial cells cultured with 33.0mmol/L D-glucose(high concentration glucose)were set as high concentration glucose induced group,which treated by DMSO were set as control group.High concentration glucose induced group was treated by 3kinds of PPAPγagonists,including pioglitazone,GW9662 and genipin.Effects of 3kinds of drugs on NO and ROS in vascular endothelial cells were assessed by using the fluorescent probes of NO and superoxide anion.The expression level of uncoupling protein 2was determined by Western blot.Results There were significant differences of the levels of NO and ROS between high concentration glucose induced group and control group induced by DMSO(P〈0.05).Among 3kinds of drugs,pioglitazone had the strongest effects on the levels of ROS,NO and uncoupling protein 2(P〈0.05).Conclusion PPARγcan significantly alleviate the generation of ROS in vascular endothelial cells induced by high concentration glucose,which plays a role mainly through the up-regulation of uncoupling protein 2.

关 键 词:血管内皮细胞 活性氧 过氧化物酶体增殖物受体γ 高糖介导 

分 类 号:R541.3[医药卫生—心血管疾病]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象