论文部分内容阅读
目的:研究花生四稀酸代谢产物EET对神经血管单元的调控作用及对脑缺血再灌注损伤的神经保护机制。方法:通过敲除EET的水解酶基因升高内源性EET或应用外源性EET,研究EET对局灶性脑缺血小鼠及氧糖剥夺(OGD)损伤的神经血管单元组成细胞的作用及机制。结果:EET减轻脑缺血再灌注小鼠的脑梗死体积和神经元调亡;明显抑制OGD诱导的培养脑皮
Objective: To study the regulation of arachidonic acid metabolite EET on neurovascular units and the neuroprotective mechanism of cerebral ischemia-reperfusion injury. Methods: EET was used to investigate the effect of EET on the expression of neuronal vasculature cells in focal cerebral ischemia and oxygen-glucose deprivation (OGD) injury by deleting endogenous EET or exogenous EET by hydrolase gene of EET And mechanism. Results: EET attenuated cerebral infarction volume and neuronal apoptosis in mice with cerebral ischemia and reperfusion; and significantly inhibited the growth of cultured cerebral cortex