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

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。

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

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 and 100 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.