一氧化氮在17-β雌二醇抑制血管平滑肌细胞增殖和原癌基因c-fos表达中的作用  

17β-Estradiol inhibits vascular smooth muscle cell proliferation and c-fos expression: role of nitric oxide

作　　者：杨丹[1] 谈智[1] 刘培庆[1] 潘敬运[1] 王庭槐[1] 

机构地区：[1]中山医科大学生理学教研室,广州510080

出　　处：《生理学报》2002年第1期17-22,共6页Acta Physiologica Sinica

基　　金：ThisprojectwassupportedbyagovernmentgrantfromtheMinistryofHealth (No 5 2 2 10 10 19)

摘　　要：实验利用大鼠血管平滑肌细胞 (vascularsmoothmusclecells ,VSMC)作为模型 ,观察 17 β雌二醇 (E2 )对VSMC增殖和原癌基因c fos表达的影响 ,并探讨VSMC源性一氧化氮 (NO)在其中的作用。检测指标包括NO释放的测定、细胞计数、3　H Tdr掺入、噻唑蓝 (MTT)测定和c fosmRNA表达。结果显示 ,E2 ( 10 12 ～ 10 -8mol/L)呈浓度依赖性地促进VSMC中NO的释放 ;10 -8mol/LE2 能明显抑制 10 %小牛血清 (FCS)和 10 -7mol/L内皮素 1(ET 1)诱导的细胞增殖和DNA合成 ,E2 的抑制作用均可被雌激素受体 (ER)拮抗剂tamoxifen ( 10 -7mol/L)和一氧化氮合酶抑制剂L NAME( 10 -6 mol/L)明显减轻 ;E2 ( 10 -8mol/L)可明显抑制 10 -7mol/LET 1诱导的VSMCc fos表达 ,这种抑制作用可被L NAME ( 10 -6 mol/L)明显减轻。这些结果提示E2 能抑制VSMC增殖和原癌基因c fos表达 ,这和促进VSMC的NO释放密切相关 。Rat vascular smooth muscle cells (VSMC) were used to study the effect of 17β estradiol (E 2) on cellular proliferation (cell counting), DNA synthesis ( 3 H thymidine incorporation) , MTT, c fos mRNA expression and nitric oxide (NO) release. The results obtained showed that E 2(10 -12 ～10 -8 mol/L) induced NO release from VSMC in a concentration dependent manner; 10 -8 mol/L E 2 significantly inhibited VSMC cellular proliferation and DNA synthesis induced by 10% FCS and 10 -7 mol/L ET 1, which was obviously reversed by 10 -7 mol/L tamoxifen and 10 -6 mol/L L NAME; after a pretreatment for 24 hours, 10 -8 mol/L E 2 significantly inhibited VSMC c fos mRNA expression induced by 10 -7 mol/L ET 1, which was also obviously reversed by 10 -6 mol/L L NAME . These results suggest that the inhibitory effects of E 2 on VSMC cellular proliferation and c fos mRNA expression are closely related with NO release in VSMC, which is, at least, partly medicated by ER .

关 键 词：血管平滑肌细胞 雌激素 一氧化氮 一氧化氮合酶 C-FOS 原癌基因表达 细胞增殖 抑制作用 

分 类 号：R363[医药卫生—病理学]