绿原酸对过氧化氢诱导内皮细胞凋亡的保护作用

目的探讨绿原酸对体外过氧化氢诱导人脐静脉内皮细胞凋亡的影响及机制。方法体外培养的人脐静脉内皮细胞株传代后进行实验,分为(A)正常对照组、(B)绿原酸组(30μmol.L-1)、(C)H2O2损伤组、(D)绿原酸+H2O2组。检测细胞线粒体膜电位;Hoechst33258荧光染色检测细胞凋亡;RT-PCR检测不同组内皮细胞Caspase-3和Bcl-2基因的表达。结果与正常对照组比较,过氧化氢(400μmol.L-1)能明显的造成内皮细胞的凋亡(P<0.05),绿原酸(30μmol.L-1)可降低过氧化氢引起的内皮细胞凋亡,表现为细胞凋亡率减少(P<0.05),线粒体膜电位增加,Bcl-2的表达增强,Caspase-3的表达减弱。结论绿原酸可抑制过氧化氢引起的内皮细胞凋亡,其作用机制可能与保护线粒体膜电位,促进凋亡抑制基因Bcl-2的表达及抑制Caspase-3的表达有关。

Protective effect of chlorogenic acid on endothelial cells apoptosis induced by H2O2

Aim To investigate the effect of chlorogenic acid on the injury of human umbilical vein endothelial cells(HUVEC)induced by hydrogen peroxide in vitro and to explore its underlying mechanism.Methods The HUVEC line was subcultured in vitro and used for experiment.This study was conducted as follows:(A)normal control group,(B)chlorogenic acid group(30 μmol·L-1),(C)hydrogen peroxide injury group,(D)chlorogenic acid and hydrogen peroxide group.mitochondrial membrance potential was detected;Cell apoptosis were observed by Hoechst33258;Endothelial Cells Caspase-3 and Bcl-2 gene changes were detected by RT-PCR.Results Comparied with normal control group,H2O2(400 μmol·L-1)can obviously damage endothelial cells(P<0.05),while chlorogenic acid(30 μmol·L-1)can disturb this damage,which involves a reduction in the rate of apoptosis(P<0.05),an increase in mitochondrial membrance potential,an increase the gene expression of Bcl-2,and the inhibition to the gene expression of Caspase-3.Conclusion Chlorogenic acid can inhibit the apoptosis of vascular endothelial cells induced by H2O2,and its mechanism may be related to the protection of mitochondrial membrance potential,the increase in the gene expression of Bcl-2 and the inhibition to the gene expression of Caspase-3.