17β-雌二醇诱导血管内皮细胞一氧化氮释放及其与细胞内钙的关系  

17β-estradiol induced nitric oxide release in vascular endothelial cells

作　　者：王庭槐[1] 杨丹[1] 刘培庆[1] 龚素珍[1] 鲁伟[1] 潘敬运[1] 

机构地区：[1]中山医科大学生理教研室,广州510089

出　　处：《生理学报》2000年第6期479-482,共4页Acta Physiologica Sinica

基　　金：surpported by Government Grant for the Ministry of Health(No.522101019)

摘　　要：利用小牛胸主动脉内皮细胞 (BAECs)作为模型 ,观察 17β 雌二醇 (E2 )对BAECs一氧化氮 (NO)释放、一氧化氮合酶 (eNOS)mRNA表达和细胞内钙 ([Ca2 +]i)的影响 ,以及雌激素受体 (ER)拮抗剂tamoxifen和NOS抑制剂(L NAME)的作用。结果显示 ,E2 (10 -12 ～ 10 -8mol/L)呈浓度依赖性促进BAECs中NO的释放 ,以 10 -8mol/L浓度E2 处理BAECs 48h ,可见eNOSmRNA表达明显增加 ,这些作用均可被tamoxifen (10 -7mol/L)和L NAME (10 -6mol/L)明显抑制 ;E2 (10 -8mol/L)处理 48h可使BAECs静息 [Ca2 +]i 和ATP诱导的 [Ca2 +]i 上升幅度均显著增加。提示E2 能促进BAECs的NO释放和eNOSmRNA表达 ,该作用至少部分通过ER介导 ,并可能与细胞内钙动员有关。Bovine aortic endothelial cells (BAECs) were used to study the effect of 17β estradiol (E 2) on nitric oxide (NO) release, nitric oxide synthase (eNOS) mRNA expression and intracellular free calcium con^cen^tration ([Ca 2+ ] i) and modulation of the effect of E 2 by estrogen receptor (ER) antagonist tamoxifen and NOS inhibitor L NAME. E 2 (10 -12 ～10 -8 mol/L) induced NO release of BAECs in a concentration dependent manner and the abundant expression of eNOS mRNA in BAECs increased obviously after treatment with E 2 (10 -8 mol/L) for 48 h. These effects were evidently inhibited by tamoxifen (10 -7 mol/L) and L NAME (10 -6 mol/L). Furthermore treatment with E 2 (10 -8 mol/L) for 48 h significantly increased the resting [Ca 2+ ] i and the rise of [Ca 2+ ] i induced by ATP in BAECs. These results suggest that E 2 induced NO release and eNOS mRNA expression in BAECs may be mediated by ER and related to calcium mobilization. [WT5HZ]

关 键 词：内皮细胞 雌激素 一氧化氮 一氧化氮合酶 钙 

分 类 号：Q463[生物学—生理学]