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。
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 DttFC -DA fluorescence, and mitochon- drial 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 nor- mal cell secretion of hPAE via inhibition of the ROS in hPAE mitochondria induced by CSE.
出处
《中华中医药学刊》
CAS
2013年第4期798-800,共3页
Chinese Archives of Traditional Chinese Medicine
基金
浙江省中医药科技计划项目(2010ZB092)
关键词
氧化应激
肺动脉内皮细胞
红景天苷
活性氧族(ROS)
salidroside
oxidative stress
pulmonary artery endothelial cells （ hPAE ）
reactive oxygen species （ROS）
