论文部分内容阅读
目的:研究脂质过氧化损伤后内皮细胞产生环磷腺苷酸(CAMP)、一氧化氮(NO)的量的变化及NO形成过程中第二信使CAMP的作用.方法:用联胺、硒作为氧化剂及抗氧化剂,应用光镜、电镜、丙二醛测定方法观察内皮细胞脂质过氧化损伤程度;用放免方法测细胞内CAMP含量,GRIESS方法测培养液中NO代谢产物亚硝酸盐(NO－2)的含量.结果:联胺可以引起内皮细胞脂质过氧化损伤,低、中联胺浓度组CAMP含量明显升高,硒保护组比损伤组降低(P＜0.01),高联胺浓度组CAMP降低,加硒组有所回升(P＜0.05).但NO含量随联胺浓度升高增多(P＜0.01),硒可使NO升高程度减小(P＜0.05).CAMP升高因素可使内皮细胞(EC)产生NO增多.结论:轻中度或早期动脉硬化(AS)病变可能是通过CAMP介导的;CAMP可能在NO合成中起一定作用.以往NO“减少”的报道可能是由于产生的NO被自由基等灭活导致NO的活性降低“,”Objective:To further understand the mechanism whereby lipoperoxide alters endothelial cell (EC) properties and make it clear whether the decrease effect of NO in atherosclerosis (AS) is caused by the decrease of NO content or activity. Methods:NO - 2 (the essential metabolite of NO) and cAMP were measured by Griess method and radioimmunological assay after the addition of diamide. In another series of experiments, cAMP elevating agents IBMX、Isoprenalin、ALF 4were added and NO - 2 in the medium was ...