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目的 研究局灶脑缺血 /再灌注Wistar大鼠原癌基因c fos、c jun表达在缺血性脑损害中可能的作用机制。 方法 采用线栓法制备大鼠局灶脑缺血 /再灌注模型 ,于缺血 1 5h再灌注 4h、2 4h、72h观察c fos、c jun表达及神经元坏死、凋亡的变化规律。结果 再灌注 4hc fos、c jun及神经元凋亡明显升高 (P <0 0 1) ,c fos和c jun阳性蛋白表达在 4h达高峰 (P <0 0 1) ,随后逐渐下降 (P <0 0 5 ) ,但仍高于正常组 ;神经元凋亡细胞数在再灌注 2 4h达高峰 (P <0 0 1) ,72h开始下降 (P <0 0 1) ;神经元坏死在再灌注各时相点无显著性差异 (P >0 0 5 )。结论 c fos和c jun异常表达与神经元坏死、凋亡密切相关
Objective To investigate the possible mechanism of c-fos and c-jun expression in ischemic brain damage in focal cerebral ischemia / reperfusion Wistar rats. Methods The model of focal cerebral ischemia / reperfusion was established by thread occlusion. The expressions of c fos, c jun and the changes of neuron apoptosis and necrosis were observed at 4h, 24h, 72h after ischemia for 15 hours. Results The expressions of c fos and c jun were significantly higher at 4h after reperfusion (P <0.01), and then gradually decreased at 4h (P < The number of apoptotic neurons reached the peak at 24 hours after reperfusion (P <0.01), and began to decrease at 72 hours (P <0.01). Necrosis of the neurons in reperfusion There was no significant difference at each time point (P> 0.05). Conclusion The abnormal expressions of c fos and c jun are closely related to neuronal necrosis and apoptosis