Estrogen & Vit E on Nitric Oxide & Inflammation in Postmenopausal Women

人类的动脉粥样硬化与 发炎。提高一氧化氮(NO)生物活性的治疗方法 可能会减少血管内促炎症蛋白的合成 WALL通过抑制靶基因的转录激活。AS 雌激素和维生素E治疗改善血管内皮细胞一氧化氮 生物活性，我们给马匹注射结合雌激素(CEE) .每天625毫克，每天维生素E 800国际单位，及其组合，各 对28名绝经后妇女进行为期6周的随机试验， 双盲、3期交叉研究。臂动脉 前臂缺血(A)后血流介导的扩张(FMD) 内皮细胞NO)和血清炎症细胞水平的生物测定 黏附分子E-选择素、细胞间黏附分子 (ICAM-1)和血管细胞黏附分子(VCAM-1) 每次治疗前和治疗后测量。所有治疗方法都有所改进 口蹄疫(均为P&lt；0.001)和类似程度(经方差分析P=0.267)， 但不包括硝酸甘油的扩张器反应(均为P&lt；0.235)。 然而，只有包括CEE在内的疗法显著降低了水平 细胞黏附分子。与各自的基线比较 CEE时E-选择素水平降低(-13+/-15%， P&lt；0.001)，CEE+维生素E(-20+/-17%，P&lt；0.001)， 但不是单独的维生素E(+3+/-28%)。ICAM-1水平为 CEE降低(-7+/-17%，p&lt；0.05)，CEE与维生素E联合 (-7+/-19%，p&lt；0.05)，但不是单独的维生素E。血管细胞黏附分子-1水平 下降了CEE(-6+/-21%，p&lt；0.01)，但没有下降 与维生素E(-2+/-21%)结合，或单独使用维生素E (-3+/-14%)。不同疗法之间的差异对 E-选择素(P&lt；0.001经方差分析)。我们的结论是，治疗 改善血管内皮细胞一氧化氮的作用可能无法与之相比 血管炎症的标记物，提示 雌激素在绝经后的抗炎作用机制 女人。

Atherosclerosis in humans is associated with inflammation. Therapies that increase nitric oxide (NO) bioactivity may reduce synthesis of proinflammatory proteins within the vessel wall by inhibiting transcriptional activation of target genes. As estrogen and vitamin E therapies improve endothelial NO bioactivity, we administered conjugated equine estrogen (CEE) .625 mg daily, vitamin E 800 IU daily, and the combination, each for 6 weeks to 28 postmenopausal women in a randomized, double-blind , 3-period crossover study. Brachial artery flow-mediated dilation (FMD) following forearm ischemia (a bioassay for endothelial NO), and serum levels of inflammatory cell adhesion molecules E-selectin, intercellular adhesion molecule (ICAM-1), and vascular cell adhesion molecule (VCAM-1) were measured before and after each therapy. All therapies improved FMD (all P<0.001) and to a similar degree (P=0.267 by ANOVA), but not the dilator response to nitroglycerin (all P<0.235). However, only therapies including CEE significantly reduced levels of cell adhesion molecules. Compared with respective baseline values, levels of E-selectin were lowered on CEE (-13+/-15%, p<0.001), CEE combined with vitamin E (-20+/-17%, p<0.001), but not vitamin E alone (+3+/-28%). Levels of ICAM-1 were lowered by CEE (-7+/-17%, p<.05), CEE combined with vitamin E (-7+/-19%, p<0.05), but not vitamin E alone. Levels of VCAM-1 were lowered by CEE (-6+/-21%, p<0.01), but not by CEE combined with vitamin E (-2+/-21%), or vitamin E alone (-3+/-14%). Differences among therapies were highly significant for E-selectin (P<0.001 by ANOVA). We conclude that therapies that improve endothelial NO may not have comparable effects on markers of vascular inflammation, suggesting a primary anti-inflammatory mechanism for estrogen in postmenopausal women.