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目的探讨缺血再灌注后蛋白聚集与大鼠皮层神经元延迟性死亡的关系。方法采用20 min全脑缺血的大鼠模型。按照再灌注时间分为5组:假手术组,0.5 h恢复组,4 h恢复组,24h恢复组,72 h恢复组。采用HE染色光镜下观察缺血再灌注后皮层神经元的延迟性死亡。应用透射电子显微镜观察细胞胞浆内蛋白聚集物。Westernblot分析泛素蛋白标记的蛋白聚集物在神经元内的含量变化。结果HE染色显示缺血再灌注72 h后,可见部分皮层神经元死亡。透射电镜显示再灌注4 h后神经元的胞浆内形成了蛋白聚集物。Western blot分析显示,与假手术组相比较,再灌注后0.5 h被泛索标记的蛋白聚集物便开始显著增加,再灌注后4 h和24 h达到峰值,再灌注后72 h含量开始减少。但仍然高于假手术组。结论蛋白聚集是导致缺血再灌注后神经元延迟性死亡的一个重要因素。
Objective To investigate the relationship between protein accumulation and delayed neuronal death in rat cortical neurons after ischemia-reperfusion. Methods 20 min global cerebral ischemia rat model. According to the reperfusion time, the rats were divided into 5 groups: sham operation group, 0.5 h recovery group, 4 h recovery group, 24 h recovery group and 72 h recovery group. The delayed neuronal death after ischemia-reperfusion was observed under HE staining. The cytoplasmic protein aggregates were observed by transmission electron microscopy. Western blot analysis of ubiquitin protein-labeled protein aggregates in neurons content changes. Results HE staining showed that after 72 hours of ischemia-reperfusion, some cortical neurons died. Transmission electron microscopy revealed protein aggregates within the cytoplasm of neurons 4 h after reperfusion. Western blot analysis showed that compared with the sham-operated group, the protein aggregates began to increase markedly at 0.5 h after reperfusion and peaked at 4 h and 24 h after reperfusion, and began to decrease at 72 h after reperfusion. But still higher than sham group. Conclusion Protein aggregation is an important factor leading to delayed neuronal death after ischemia-reperfusion.