摘要
目的:探讨虾青素对体外氧化应激诱导人外周血内皮祖细胞凋亡的影响及机制。方法:体外培养人外周血单核细胞源的内皮祖细胞,分为对照组、模型组(叔丁基过氧化氢100μmol/L)、虾青素+叔丁基过氧化氢组(虾青素0.1、1.0、10.0nmol/L预处理24h后,再加终浓度为100μmol/L的叔丁基过氧化氢溶液继续培养6h)。MTT法检测细胞存活率;DAPI染细胞检测细胞凋亡率;比色法检测半胱氨酸天冬氨酸蛋白酶(Caspase-3)活性;JC-1法测定线粒体膜电位。结果:与对照组比较,叔丁基过氧化氢(100μmol/L)能明显造成内皮祖细胞的凋亡(P<0.05)。虾青素可降低叔丁基过氧化氢引起的内皮祖细胞凋亡,表现为细胞凋亡率减少(P<0.05),线粒体膜电位增加,Caspase-3表达减弱。结论:ASX通过保护线粒体膜电位,下调Caspase-3活性,最终起到抗氧化应激诱导的内皮祖细胞凋亡。
Objective： To investigate the effect of astaxanthin on the injury of endothelial progenitor cell （EPCs） induced by oxidative stress in vitro and to explore its underlying mechanism. Method： EPCs were exposed to 100 umol/L tBHP with various concentrations of astaxanthin pre-incubated, then the cell viability was measured by MTT method, the level of reactive oxygen species （ROS） was determined by DCFH-DA method,the changes of mitochondrial membrane potential （MMP） and apoptosis ratio were detected by JC-1 method and DAPI method. The changes of EPCs Caspase-3 activity were detected. Result： Compared with control group, 100 umol/L tBHP obviously damaged EPCs （P〈0.05）, while astaxanthin disturbed this damage, which involved the significantly increased cells viability, decreased the ROS level and the percentage of apoptosis （P〈0.05） obviously, increased MMP and linhibitition of the Caspase-3 activity. Conclusion Astaxanthin inhibits endothelial progenitor cell apop- tosis induced by oxidative stress, and its mechanism may improve the mitochondrial function, and has further biol- ogy effects.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2014年第4期349-353,共5页
Journal of Clinical Cardiology
基金
湖北省自然科学基金重点项目(No:2010CDA036)
关键词
氧化应激
内皮祖细胞
虾青素
细胞凋亡
线粒体膜电位
oxidative stress endothelial progenitor cells astaxanthin cell apoptosis mitochondrial mem-brane potential
