论文部分内容阅读
目的 观察 17β 雌二醇对大鼠肺血管内皮细胞一氧化氮合酶 (NOS)活性的影响及雌激素受体在其中的作用。方法 用贴壁法和无酚红 16 40培养基培养大鼠肺血管内皮细胞 ,在不同浓度的 17β 雌二醇 (伴或不伴有雌激素受体拮抗剂代莫昔芬 )作用下 ,观察一定时间内内皮细胞的NOS活性及一氧化氮 (NO)的产量。放射配体结合分析技术检测内皮中的雌激素受体。结果 (1) 1～ 10nmol的 17β 雌二醇作用 8～ 2 4h ,内皮细胞的NO产量显著增加 (vs对照 P<0 .0 5 ) ,10nmol的 17β 雌二醇作用 8～ 2 4hNOS活性显著增强 (与对照比 ,8h ,P<0 .0 5 ;16h ,2 4h ,P<0 .0 1)。 (2 )大鼠肺血管内皮细胞中存在雌激素受体。 (3)雌激素受体拮抗剂他莫昔芬能显著抑制雌激素的上述作用 (P <0 .0 1)。结论 17β 雌二醇能增强大鼠血管内皮细胞的NOS活性和NO产量 ,该作用由雌激素受体介导 ,可能是雌激素降低血管阻力、抑制动脉粥样硬化作用的重要机理之一。
Objective To observe the effect of 17β-estradiol on the activity of nitric oxide synthase (NOS) in rat pulmonary vascular endothelial cells and the role of estrogen receptor in it. Methods Rat pulmonary vascular endothelial cells were cultured with adherent method and phenol red-free 1640 medium under the action of different concentrations of 17β-estradiol with or without estrogen receptor antagonist moxifloxacin Endothelial NOS activity and nitric oxide (NO) production in a certain period of time. Radioligand binding assay detects estrogen receptors in the endothelium. RESULTS: (1) The NO production of endothelial cells increased significantly (P <0.05) with the effect of 1 ~ 10 nmol of 17β-estradiol for 8 ~ 24 h and the activity of NOS increased markedly after 8 ~ 24 h (Compared with the control, 8h, P <0.05; 16h, 24h, P <0.01). (2) There is estrogen receptor in rat pulmonary vascular endothelial cells. (3) Tamoxifen, an estrogen receptor antagonist, can significantly inhibit the above effects of estrogen (P <0.01). Conclusion 17β-estradiol can enhance the NOS activity and NO production in rat vascular endothelial cells. This effect is mediated by estrogen receptor, which may be one of the important mechanisms of estrogen lowering vascular resistance and inhibiting atherosclerosis.