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血管紧张素Ⅱ1型受体(AT1R)阻断剂可降低高血压患者缺血性中风和脑部炎症的发生率,并在动物模型中观察到减轻损伤的效应。尽管血细胞(BC)和血管内皮细胞(EC)的AT1R可被血管紧张素Ⅱ激活并诱发炎症反应,但BC和EC中表达的AT1R在血管紧张素引发高血压后对缺血再灌注(I/R)脑损伤作用如何尚不明了。为了评估BC和EC中的AT1R对I/R引起
Angiotensin II type 1 receptor (AT1R) blockers reduce the incidence of ischemic stroke and brain inflammation in hypertensive patients and observe the effect of lesion injury in animal models. Although AT1R in blood cells (BC) and vascular endothelial cells (ECs) is activated by angiotensin II and induces an inflammatory response, AT1R expressed in BC and EC contributes significantly to ischemia / reperfusion (I / R) What is the role of brain damage is not yet clear. To assess AT1R in BC and EC caused by I / R