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许多临床及基础研究显示雌激素对脑缺血具有保护作用 ,它能通过多种途径增加缺血区的血流量 ,减少再灌注损伤 ,有利于残存的神经元恢复功能。本文主要从分子机制方面阐述 ,雌激素能抑制缺血区肿瘤坏死因子 α(TNF α)等炎性细胞因子及粘附分子的表达 ;能作用于钙通道抑制钙离子超载和兴奋性氨基酸释放 ;诱发BCL 2等抗凋亡蛋白的表达 ,而且各途径之间关系密不可分。明确雌激素对脑缺血保护作用的确切机制 ,将更好地指导其临床应用
Many clinical and basic studies have shown that estrogen has a protective effect on cerebral ischemia. It can increase blood flow in the ischemic area and reduce the reperfusion injury in a variety of ways, which is conducive to the survival of the remaining neurons. This article mainly elaborates on the molecular mechanism. Estrogen can inhibit the expression of inflammatory cytokines and adhesion molecules such as tumor necrosis factor-alpha (TNF-alpha) in the ischemic area, inhibit calcium overload and release of excitatory amino acids through calcium channel, Induced the expression of anti-apoptotic protein BCL 2, and the relationship between the various channels are inseparable. A clear mechanism of estrogen’s protective effect on cerebral ischemia will be better to guide its clinical application