异丙酚在第三丁基过氧化氢诱导脐静脉内皮细胞氧化应激中的保护作用  

The protective effect and mechanism of propofol on oxidative stress induced by tert-butyl hydroperoxide of human umbilical vein endothelial cells

作　　者：王乃田[1] 肖华平[1] 肖金仿[1] 古妙宁[1] 

机构地区：[1]南方医科大学南方医院麻醉科,广州市510515

出　　处：《实用医学杂志》2011年第9期1523-1525,共3页The Journal of Practical Medicine

基　　金：国家自然科学基金资助项目(编号:30872431)

摘　　要：目的:研究异丙酚对第三丁基过氧化氢(t-BHP)诱导的脐静脉内皮细胞(HUVECs)氧化应激的保护作用和机制。方法:体外培养的HUVECs分为对照组、异丙酚组、t-BHP组、异丙酚预处理+t-BHP组,给予相应处理后,Westernblot检测p38MAPK磷酸化水平变化,RT-PCR检测iNOS、eNOS表达。结果:t-BHP处理后,能显著诱导p38MAPK磷酸化,激活iNOS、eNOS表达,而异丙酚预处理后能减轻这些变化。结论:异丙酚通过抑制p38MAPK,减少iNOS、eNOS表达,减轻氧化应激从而起到保护HUVECs的作用。Objective To investigate the protective effect and mechanism of propofol on human umbilical vein endothelial cells （HUVECs） following oxidative stress induced by ten-butyl hydroperoxide （t-BHP）. Methods Cultured HUVECs were divided into four groups： control group, t-BHP group, propofol group, and pre-ineubated with propofol and treated with t-BHP group. Levels of p38 MAPK phosphorylation were measured by Western blot, and expressions of iNOS and eNOS were measured by RT-PCR. Results The phosphorylation of p38 MAPK was significantly induced, and the expressions of iNOS and eNOS were significantly increased while treated with t-BHP, which could be attenuated by propofol. Conclusions By inhibiting p38MAPK and decreasing iNOS and eNOS expression, propofol could protect HUVECs from oxidative stress.

关 键 词：二异丙酚 氧化应激 脐静脉内皮细胞 P38丝裂原活化蛋白激酶 一氧化氮合酶 

分 类 号：R96[医药卫生—药理学]