中文摘要：

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。

英文摘要：

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.