血脂康对氧化型低密度脂蛋白致人脐静脉内皮细胞凋亡的拮抗作用  

The antagonistic effect of Xuezhikang on apoptosis of human umbilical vein endothelial cells induced by oxidized low density lipoprotein

作　　者：匡泽民[1] 奉淑君 唐欣颖 王瑛 程文立 KUANG Zemin;FENG Shujun;TANG Xinying;WANG Ying;CHENG Wenli(Department of Hypertension,Beijing Anzhen Hospital of Capital Medical University,Beijing 100029,China;Department of Cardiology,Chenzhou Hospital Affiliated to University of South China,Chenzhou,Hunan 423000,China;Department of Cardiology,The Second Affiliated Hospital of Henan University of Science and Technology,Luoyang,Henan 471000,China)

机构地区：[1]首都医科大学附属北京安贞医院高血压科,北京市100029 [2]南华大学附属郴州医院心血管内科,湖南省郴州市423000 [3]河南科技大学第二附属医院心血管内科,河南省洛阳市471000

出　　处：《中国动脉硬化杂志》2019年第7期573-578,共6页Chinese Journal of Arteriosclerosis

基　　金：中国中青年临床研究基金(2017-CCA-VG-016);“互联网+专家团队”驱动的高血压分级诊疗模式示范应用(2018-TG-03)

摘　　要：目的研究血脂康对氧化型低密度脂蛋白(ox-LDL)诱导的人脐静脉内皮细胞(HUVEC)凋亡的影响及其可能机制。方法体外培养HUVEC,实验分为空白对照组、ox-LDL组、ox-LDL+不同浓度(25 mg/L、50 mg/L和100 mg/L)血脂康组。采用细胞增殖及毒性检测试剂盒检测细胞存活率,Annexin V-FITC/PI双染细胞检测细胞凋亡,活性氧检测试剂盒检测细胞内活性氧(ROS),蛋白免疫印迹分析细胞色素C(CytC)、Caspase-3和PARP-1蛋白的表达情况。结果血脂康(25 mg/L、50 mg/L和100 mg/L)可拮抗ox-LDL诱导的HUVEC凋亡、ROS水平增加,100 mg/L血脂康可下调细胞CytC、Caspase-3和PARP-1蛋白的表达。结论血脂康可通过减少ROS形成而抑制CytC释放、减少Caspase-3和PARP-1活化抑制线粒体凋亡途径启动,拮抗ox-LDL诱导的血管内皮细胞凋亡。Aim To investigate the effect of Xuezhikang( XZK) on apoptosis induced by oxidized low density lipoprotein( ox-LDL) and its possible mechanism. Methods Human umbilical vein endothelial cells( HUVEC) were cultured and divided into three groups,namely control group,ox-LDL group and ox-LDL+XZK( different dosages) groups.Cell counting kit-8 was used to test cell survival,Annexin V-FITC/PI apoptosis detection kit was used to count apoptotic rate of HUVEC among different groups,reactive oxygen species( ROS) were detected by ROS assay kit,expression of cytochrome C( CytC),caspase-3 and PARP-1 were analyzed by Western blot. Results XZK( 25 mg/L,50 mg/L and100 mg/L) showed an antagonistic effect on apoptosis and ROS production of HUVEC induced by ox-LDL,and 100 mg/L XZK downregulated the protein expression of CytC,caspase-3 and PARP-1. Conclusion XZK reduces ROS production,leading to less expression of CytC,caspase-3 and PARP-1,thus prevents mitochondrial apoptotic signaling from activating,and eventually protects HUVEC from apoptosis.

关 键 词：血脂康 氧化型低密度脂蛋白 氧化应激 细胞凋亡 动脉粥样硬化 

分 类 号：R363[医药卫生—病理学] R5[医药卫生—基础医学]