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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 study the effect of salidroside on mitochondrial ROS and cell secretory function of human pulmonary artery endothelial cells under oxidative stress and its molecular mechanism. Methods: ROS was induced by human pulmonary artery endothelial cells (hPAE) using cigarette smoke extract (CSE), hPAE was treated with salidroside, and the levels of NOS, ET-1 and VGGF in hPAE treated with salidroside and CES were detected by ELISA Changes of mitochondrial ROS and mitochondrial membrane potential were detected by DCFH-DA and Rh123. Results: The fluorescence intensity of DCFH-DA in mitochondrial ROS of CSE group was higher than that in physiological water group. The synthesis of NOS, ET-1 and VEGF in CSE group was higher than that in CSE + salidroside group and saline group. The mitochondrial membrane potential of CSE group was higher than CSE + salidroside group and saline group. The fluorescence intensity of DCFH-DA and DiBAC4 in mitochondrial ROS of CSE + salidroside group was lower than that of CSE group and close to normal saline group. Conclusion: Salidroside can inhibit CSE-induced human hPAE mitochondrial ROS generation, restore mitochondrial membrane potential, reduce the synthesis of NOS, ET-1 and VEGF, so as to protect the secretion of hPAE cells under oxidative stress.