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The pathways by which mild hypothermia inhibits neuronal apoptosis following ischemia/reperfusion injury

机译:亚低温抑制缺血/再灌注损伤后神经元凋亡的途径

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Several studies have demonstrated that mild hypothermia exhibits a neuroprotective role and it can inhibit endothelial cell apoptosis following ischemia/reperfusion injury by decreasing casp-ase-3 expression. It is hypothesized that mild hypothermia exhibits neuroprotective effects on neurons exposed to ischemia/reperfusion condition produced by oxygen-glucose deprivation. Mild hypothermia significantly reduced the number of apoptotic neurons, decreased the expression of pro-apoptotic protein Bax and increased mitochondrial membrane potential, with the peak of anti-apoptotic effect appearing between 6 and 12 hours after the injury. These findings indicate that mild hypothermia inhibits neuronal apoptosis following ischemia/reperfusion injury by protecting the mitochondria and that the effective time window is 6-12 hours after ischemia/reperfusion injury.
机译:多项研究表明,温和的低温表现出神经保护作用,并且可以通过降低casp-ase-3的表达来抑制缺血/再灌注损伤后内皮细胞的凋亡。假设轻度低温对暴露于由氧-葡萄糖剥夺产生的局部缺血/再灌注条件的神经元表现出神经保护作用。轻度的亚低温显着减少凋亡神经元的数量,降低促凋亡蛋白Bax的表达并增加线粒体膜电位,在损伤后6至12小时出现抗凋亡作用的高峰。这些发现表明,温和的低温通过保护线粒体来抑制缺血/再灌注损伤后的神经元凋亡,并且有效时间窗口是缺血/再灌注损伤后的6-12小时。

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