摘要
目的:探讨雌激素及其受体对血管内皮细胞一氧化氮表达的影响。方法:采用无酚红的1640培养基培养大鼠血管内皮细胞,给予不同浓度的17β-雌二醇(17β-E2)用贴块法和无酚红的1640培养基建立肺血管内皮细胞模型,观察不同浓度的17β-E2(伴或不伴有雌激素受体拮抗剂tamoxifen)作用下血管内皮细胞一氧化氮合酶(nitric-oxidesynthase,NOS)的活性及一氧化氮的产量。NOS的活性用血红蛋白酶法检测,Griess法检测一氧化氮的产量,放射配体结合分析法检测血管内皮中的雌激素受体。结果:一定浓度的17β-E2作用8~24h血管内皮细胞一氧化氮的产量显著增加犤1nmol/L,10nmol/L,17β-E2同对照组相比(t=1.221;P<0.05)犦;NOS活性显著增加(t=1.722,P<0.05,t=3.680-4.174,P<0.01);放射配体结合分析法在血管内皮中检测到雌激素受体;雌激素受体拮抗剂能显著抑制雌激素的上述作用。结论:17β-雌二醇能通过雌激素受体途径增强血管内皮细胞的活性,这是雌激素对动脉粥样硬化防治作用的机制之一。
AIM:To investigate the effect of estrogen and its receptor antagonism on vascular endothelial expression of nitric oxide synthase(NOS). METHODS: Female rats' endothelial cells(EC) were propagated in phenol red free 1640 medium and pretreated with several different concentration 17 β estradiol(17β E2) with or without estrogen receptor antagonist tamoxifen. The production of nitric oxide was measured by Griess reaction,and the NOS activity was assessed by hemoglobin reductase.The flowcytomety was used to measure the expression of vascular cells adhension molecular.The receptor binding assay(RBA) was adopted to measure the estrogen receptors in the endothelial cells. RESULTS:Compared with the control group,the production of NO increased significantly in vascular endothelial cells under the effect of 17β E2 of certain concentration(1 nmol/L,10 nmol/L) over 8 to 24 hours(t=1.221, P < 0.05),the eNOS activity increased significantly( t=1.722, P < 0.05, t=3.680- 4.174, P< 0.01) .The existence of estrogen receptors in ECs was detected by RBA.Estrogen receptor antagonist tamoxifen significantly inhibited the effect of estradiol mentioned above. CONCLUSION:The 17β estradiol is able to enhance the eNOS activity in vascular ECs by receptor mediated way.This mechanism may contribute to the explanation of the beneficial mechanism of estrogen in the prevention of atherosclerosis.
出处
《中国临床康复》
CSCD
2004年第6期1150-1151,共2页
Chinese Journal of Clinical Rehabilitation
基金
广东省医学科研基金立项资助项目(A2002529)~~