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脑缺血再灌注后脑损伤的发病机制较复杂,其所致病理损伤既有神经元的急性水肿、坏死,又有细胞凋亡。细胞凋亡与脑缺血再灌注损伤关系密切,且在梗死形成过程中发挥重要的作用,也是神经元迟发性死亡的主要形式。许多研究提示细胞凋亡受基因调控,与凋亡密切相关的基因ICE参与了这种迟发性死亡。本实验采用免疫组化法检测大鼠局灶性脑缺血再灌注不同时限Caspase-3蛋白的表达,旨在从分子水平探讨局灶性脑缺血再灌注损伤的机制。
The pathogenesis of brain injury after cerebral ischemia-reperfusion is more complicated, the pathological damage caused by both the acute edema and necrosis of neurons, as well as apoptosis. Apoptosis and cerebral ischemia-reperfusion injury are closely related and play an important role in the process of infarction formation, but also the main form of neuronal delayed death. Many studies suggest that apoptosis is regulated by genes. ICE, a gene closely related to apoptosis, is involved in this type of delayed death. In this study, immunohistochemistry was used to detect the expression of Caspase-3 at different time points after focal cerebral ischemia-reperfusion in rats. The aim was to explore the mechanism of focal cerebral ischemia-reperfusion injury at the molecular level.