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目的研究缺血后处理对SH-SY5Y细胞缺血再灌注损伤模型的保护作用,并初步探讨其作用机制。方法将SH-SY5Y细胞分为三组:正常组、缺血再灌注组、缺血后处理组,缺血再灌注组予以糖氧剥夺12 h后正常培养,缺血后处理组经糖氧剥夺12 h后予以3个循环的正常培养10 min/糖氧剥夺10 min,正常培养12 h后通过光镜、荧光显微镜以及细胞计数法、流式细胞术、SOD活力检测SH-SY5Y细胞的改变。结果缺血后处理组的SH-SY5Y细胞存活率较缺血再灌注组明显增加而凋亡率明显下降(P<0.01),经缺血后处理的SH-SY5Y细胞内SOD的活力较缺血再灌注组增加32.53%(P<0.05)。结论缺血后处理在细胞离体状态下可以发挥保护作用,能够降低SH-SY5Y细胞缺血再灌注损伤引起的细胞凋亡,提高细胞内SOD的活力。
Objective To study the protective effect of ischemic postconditioning on SH-SY5Y cells subjected to ischemia-reperfusion injury and to explore its possible mechanism. Methods SH-SY5Y cells were divided into three groups: normal group, ischemia-reperfusion group and ischemic postconditioning group. Rats in ischemia-reperfusion group were cultured for 12 h after oxygen-glucose deprivation, After 12 h, the cells were cultured for 3 cycles of 10 min in normal culture for 10 min, deprived of glucose and oxygen for 10 min. After 12 h of normal culture, the changes of SH-SY5Y cells were detected by light microscope, fluorescence microscope, cell counting, flow cytometry and SOD activity. Results The survival rate of SH-SY5Y cells in ischemic postconditioning group was significantly higher than that of ischemia-reperfusion group (P <0.01), and the activity of SOD in SH-SY5Y cells after ischemic postconditioning was higher than that of ischemia Reperfusion group increased by 32.53% (P <0.05). Conclusion The ischemic postconditioning can play a protective role in the state of ex vivo cells, and can reduce the apoptosis of SH-SY5Y cells induced by ischemia-reperfusion injury and increase the activity of intracellular SOD.