摘要
目的:分析脱氢表雄酮(DHEA)对CD40L刺激的人脐静脉内皮细胞(HUVECs)的一氧化氮(NO)、内皮素-1(ET-1)水平及ET-1mRNA和内皮源性NO合酶(eNOS)mRNA表达水平的影响,探讨DHEA对血管舒张的作用。方法:原代培养HUVECs,给予CD40L(1μg/m1)刺激(CD40L刺激组)和不同浓度DHEA(10-8 mol/L、10-7 mol/L、10-6 mol/L,分别为低、中、高浓度DHEA组)干预,以不作干预的培养细胞为空白对照组。采用反转录聚合酶链反应(RT-PCR)检测HUVECs的ET-1、eNOS mRNA表达,采用ELISA和硝酸还原酶法分别检测细胞培养液中NO和ET-1浓度。结果:与空白对照组比较,CD40L刺激组ET-1mRNA和ET-1浓度明显增加,eNOS mRNA和NO水平明显降低(P<0.05或P<0.01)。与CD40L组比较,不同浓度DHEA组ET-1mRNA和ET-1水平降低,eNOS mRNA和NO水平增加,以高浓度DHEA组变化最明显(P<0.05或P<0.01)。结论:DHEA能通过抑制ET-1表达和促进NO生成来保护内皮细胞的舒张血管功能。
Objective：To investigate effect of dehydroepiandrosterone（DHEA）on expression of NO,ET-1and eNOS in human umbilical vein endothelial cells（HUVECs）and influence of DHEA on diastolic function in HUVECs.Method：HUVECs were incubated with 1μg/m1CD40 Lfor 24hours with or without pretreated by different concentration of DHEA（10^-8 mol/L,10^-7 mol/L,10^-6 mol/L）.ET-1and eNOS mRNA expression were detected by RT-PCR.The levels of NO and ET-1were measured by nitrate reduction test and ELISA.Results：Compared with control group,CD40 Lincreased the mRNA expression of ET-1and level of ET-1in HUVECs（all P〈0.01）.Meanwhile,the eNOS mRNA expression and NO content in HUVECs in CD40 Lgroup were decreased（all P〈0.01）.DHEA with different concertration could down-regulate the ET-1mRNA and ET-1expression and promote the eNOS mRNA expression and NO content in HUVECs,espically the most obvious change was in 10-6 mol/L DHEA group（P〈0.05,P〈0.01）.Conclusion：DHEA could regulate vascular endothelial cells diastolic function by promoting NO generation and inhibiting ET-1expression.
出处
《微循环学杂志》
2016年第4期7-10,19,共5页
Chinese Journal of Microcirculation
基金
国家自然科学基金(81101319)
