论文部分内容阅读
目的：观察大鼠完全性前脑缺血再灌注损伤过程中海马ＣＡ１区神经元死亡的另一种形式细胞凋亡．方法：采用琼酯糖凝胶电泳及原位缺口翻译法，观察海马ＣＡ１区神经元是否有凋亡特征性改变．结果：脑缺血损伤后５ｄ，从海马ＣＡ１区神经元提取ＤＮＡ，其琼酯糖凝胶电泳呈现典型梯状结构．而采用原位缺口翻译法，发现缺血损伤后３ｄ，海马ＣＡ１区开始出现胞核染色阳性的凋亡细胞，缺血损伤后５ｄ，凋亡细胞达到高峰．结论：海马ＣＡ１区迟发性神经元死亡过程中有凋亡机制参与，这为脑缺血损伤防治开辟新的治疗途径．
OBJECTIVE: To observe the apoptosis of neurons in hippocampal CA1 area during complete forebrain ischemia-reperfusion injury in rats. Methods: The agarose gel electrophoresis and in situ nick-translation were used to observe whether neuronal apoptosis in hippocampal CA1 region was characteristic of apoptosis. Results: Five days after cerebral ischemia, DNA was extracted from neurons in hippocampal CA1 area, and the typical ladder-like structure was found in agarose gel electrophoresis. Using in situ nicked translation, it was found that nucleus stained positive apoptotic cells began to appear in hippocampal CA1 area 3 days after ischemia injury, and apoptotic cells peaked 5 days after ischemia injury. Conclusion: The mechanism of apoptosis is involved in the death of delayed neurons in hippocampal CA1 region, which opens up a new therapeutic approach for the prevention and treatment of cerebral ischemic injury.