越来越多的证据表明,炎症反应是造成脑缺血/再灌注损伤的主要原因。局部炎症因子、趋化因子及粘附分子的表达上调构成了缺血损伤向炎症性损伤转变的基础,随后白细胞向缺血区的聚集和浸润导致了继发性神经元损伤和梗死面积的扩大。 白细胞进入缺血性脑组织是一个链锁过程。链锁过程的起始是在前炎症因子白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)等的作用下,血管内皮细胞首先释 There is growing evidence that the inflammatory response is the main cause of cerebral ischemia / reperfusion injury. The up-regulation of local inflammatory cytokines, chemokines and adhesion molecules underlies the conversion of ischemic injury to inflammatory lesions, followed by the accumulation and infiltration of leukocytes into the ischemic area leading to secondary neuronal damage and an increase in infarct size . Leukocytes enter the ischemic brain tissue is a chain process. The initiation of the chaining process is initiated by the action of proinflammatory cytokines IL-1β, IL-6 and TNF-α, Cells first release