【摘要】 目的:研究红景天苷对氧化应激下人肺动脉内皮细胞线粒体ROS及细胞分泌功能的影响及其分子机制。方法:应用香烟烟雾提取液(CSE)诱导人肺动脉内皮细胞(hPAE)生成ROS,红景天苷干预hPAE,ELISA检测CES诱导、红景天苷干预的hPAE合成的NOS、ET-1、VGGF的变化,DCFH-DA、Rh123法分别检测线粒体ROS、线粒体膜电位的变化。结果:CSE组线粒体ROS的DCFH-DA的荧光强度高于生理水组,NOS、ET-1和VEGF的合成高于CSE+红景天苷组、生理盐水组;CSE组的线粒体的膜电位高于CSE+红景天苷组和生理盐水组;CSE+红景天苷组的线粒体ROS的DCFH-DA和DiBAC4的荧光强度低于CSE组,而与生理盐水组接近。结论:红景天苷可抑制CSE诱导的人hPAE线粒体ROS的生成,恢复线粒体的膜电位,降低NOS、ET-1和VEGF的合成,从而保护氧化应激下hPAE细胞的分泌功能。更多还原

【Abstract】 Objective:To investigate effects of salidroside on mitochondrial reactive oxygen species(ROS)production and cell secretion of human pulmonary artery endothelia(hPAE)and its molecular mechanism under oxidative stress.Methods:Cigarette smoke extract(CSE)was used to induce the generation of ROS in hPAE mitochondria,salidroside was used to treat hPAE induced by CES.Nitric oxide synthase(NOS),endothelin-1(ET-1)and vascular endothelial growth factor(VEGF)were determined by ELISA.Mitochondrial ROS was detected by DHFC-DA fluorescence,and mitochondrial membrane potential was detected by Rh123 fluorescence.Results:Mitochondrial DCFH-DA fluorescence intensity increased in CSE-induced hPAE.The productions of NOS,ET-1 and VEGF in CSE group were higher than those in CSE combining salidroside group and saline group.Mitochondrial membrane potential(MMP)of CSE group increased.Mitochondrial DCFH-DA and Rh123 fluorescence intensities were lower in generation of NOS,ET-1 and VEGF under oxidative stress in CSE combining salidroside group than those in CSE group,while closed to those in saline group.Conclusion:Salidroside may restore hPAE mitochondrial membrane potential owning to anti-oxidative stress,and protect normal cell secretion of hPAE via inhibition of the ROS in hPAE mitochondria induced by CSE.更多还原