摘要
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 。
Estrogen has the protective effect on cerebral ischemia in v ar ious ways. It not only can improve the regional cerebral blood flow during ische mia and rescue the remaining neurons alive, but also can reduce the injury of is chemia-reperfusion. In this article, we enumerate at the molecular level that e strogen has the properties of inhibiting the expression of VCAM and cytokines li ke TNF-α in the ischemia region, educing the overload of calcium and cytotoxic ity of EAA by modulating the calcium channels, and regulating related genes expr ession and anti-apoptosis. It is crucial for estrogen replacement therapy as a neutoprotectant clinically.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2004年第2期121-124,共4页
Chinese Journal of Clinical Pharmacology and Therapeutics
关键词
雌激素
脑缺血
神经保护作用
脑血流量
细胞凋亡
雌激素受体
estrogen
cerebral ischemia
neuroprotective
cerebral blood flow (CBF)
apoptosis, estrogen receptor