摘要
目的探讨血管紧张素-2(Ang-2)所致血管内皮细胞损伤的内在机制及合贝爽保护内皮细胞的作用。方法将体外培养的人大动脉血管内皮细胞分为对照组、Ang-2组及Ang-2+合贝爽组,三组均加入细胞培养液180μl+生理盐水20μl;在此基础上,Ang-2组加入Ang-2 10μl,使培养液中Ang-2终浓度为10-7mol/L;Ang-2+合贝爽组加入Ang-2 10μl+合贝爽10μl,使Ang-2终浓度为10-7mol/L、合贝爽终质量浓度为1 mg/L。用激光共聚焦显微镜测量各组线粒体膜电位水平。结果Ang-2组线粒体膜电位显著低于对照组(P<0.01);Ang-2+合贝爽组线粒体膜电位显著高于Ang-2组(P<0.01)。结论Ang-2通过降低线粒体膜电位而引起血管内皮细胞损伤;合贝爽可拮抗Ang-2的作用,从而保护内皮细胞,可能机制为拮抗细胞内钙超载。
Objective To explore the effects of angiotensin-2 （Ang-2） on mitochondfia membrane potential in vascular endothelial cell（VEC） and protection of herbesser. Methods VEC were divided into control group, Ang-2 group and Ang- 2 ＋ herbesser group; mitochondria membrane potential were measured by laser scanning confocal microscopy. Results Mitochondria membrane potential of Ang-2 group significantly lower than that of control group（ P 〈 0. 01 ） ; Mitochondria membrane potential of Ang-2 ＋ herbesser group significantly higher than that of Ang-2 group （ P 〈 0. 01 ）. Conclusion Ang-2 can induce obvious changes of mitochondria membrane potential in VEC and herbesser have protective effection to it.
出处
《山东医药》
CAS
北大核心
2008年第11期26-27,共2页
Shandong Medical Journal
基金
海军后勤科研基金资助项目(00-3321)
关键词
血管内皮细胞
血管紧张素-2
膜电位
线粒体
合贝爽
vascular endothelial cell （VEC）
angiotensin-2
membrane potential,mitochondria
herbesser
