红景天苷对小牛胸主动脉内皮细胞的保护作用  

Protective effects of salidroside on bovine aortic endothelial cells

作　　者：张勇[1] 颜天华[1] 袁林[1] 王秋娟[1] 

机构地区：[1]中国药科大学药学院生理教研室,南京210009

出　　处：《药学与临床研究》2009年第3期195-199,共5页Pharmaceutical and Clinical Research

摘　　要：目的:探讨红景天苷对小牛胸主动脉内皮细胞过氧化损伤?缺氧/复氧损伤的作用及其机制。方法:体外培养原代小牛胸主动脉内皮细胞,观察红景天苷对正常细胞增殖的作用及cNOS活性;用H2O2和Na2S2O4分别复制过氧化损伤模型和复制缺氧/复氧损伤模型,测定细胞活性(MTT法),并测量LDH、NO、SOD和MDA含量。结果:红景天苷明显促进正常内皮细胞增殖,给药后24小时作用明显,增加细胞裂解液中cNOS活性;在氧化损伤模型和缺氧/复氧损伤模型中,红景天苷明显提高细胞存活率,增加胞内SOD活性和NO的释放,降低培养液中LDH释放量和胞内MDA含量。结论:红景天苷能促进正常内皮细胞增殖,对缺氧/复氧损伤、过氧化损伤内皮细胞均有一定的保护作用。Objective： To investigate the protective effect and mechanism of salidroside on bovine aortic endothelial cells （BAECs） injured by hypoxia/reoxygenation or by oxidative. Methods： Primary bovine aortic endothelial cells were cultured in vitro. After preconditioning of salidroside, the changes of cell proliferation and the activity of cNOS were tested. The model of hypoxia/reoxygenation injury was induced by sodium dithionite （ Na2S2O4 ） and the model of oxidative injury was induced by hydrogen peroxide （ HEO2 ） , the viability of cell （ using MTT method） , NO, LDH, SOD and MDA were measured. Results： Salidroside could significantly promote endothelial cell proliferation, and increase the activity of cNOS. Compared with the model group of hypoxia/reoxygenation damage and oxidative damage, salidroside could obviously raise the viability of cell, NO and SOD activities, and lower LDH leakage and intracellular MDA production. Conculsion： Salidroside could significantly promote endothelial cell proliferation, can obviously protect cultured primary bovine aortic endothelial cells from hypoxia/reoxygenation damage and oxidative damage.

关 键 词：红景天苷 内皮细胞 一氧化氮 过氧化损伤 缺氧/复氧损伤 

分 类 号：R965.1[医药卫生—药理学]