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目的 探讨癫发作激发的程序性细胞死亡机制是否参与癫发作所致的神经细胞坏死过程。方法 利用Sprague Dawley大鼠 ,经腹腔内注射毛果云香碱 (pilocarpine)制作癫发作模型。在实验 2 4h和 72h ,脑灌流固定后 ,取脑进行检测。经HE和TUNEL染色 ,在光镜下 ,观察神经细胞死亡 ,并采用免疫组织化学方法检测Bax和Bcl 2基因表达。结果 癫发作 2 4h和 72h,在大鼠海马CA1 区 ,细胞损伤形态上是细胞坏死。但癫发作 72h ,在海马CA1 区 ,TUNEL阳性的坏死细胞数明显增多 ,与对照组比较差异有显著性 (P <0 .0 0 1 ) .癫发作后 72h ,Bax表达显著增高 ,与对照组比较差异有显著性 (P <0 .0 0 1 ) ,而Bcl 2表达无增高 ,Bcl 2 /Bax比值降低。结论 癫发作所致的迟发性神经细胞坏死伴有程序性细胞死亡机制
Objective To investigate whether programmed cell death induced by epileptic seizures participates in the process of neuronal necrosis caused by epileptic seizures. Methods Sprague Dawley rats were used to induce epileptic seizures by intraperitoneal injection of pilocarpine. In the experiment 2 4h and 72h, brain perfusion fixed, take the brain to detect. After HE staining and TUNEL staining, the death of nerve cells was observed under light microscope, and the expression of Bax and Bcl2 gene was detected by immunohistochemistry. Results Epileptic seizures 24 h and 72 h in the rat hippocampal CA1 area, cell damage morphology is necrosis. However, 72h after epileptic seizure, the number of TUNEL-positive necrotic cells in CA1 area of hippocampus increased significantly compared with control group (P <0.01) .The expression of Bax increased significantly at 72h after epileptic seizure, The difference between the two groups was significant (P <0.01), while the expression of Bcl 2 was not increased and the ratio of Bcl 2 / Bax was decreased. Conclusions Delayed neuronal cell necrosis caused by epileptic seizures accompanied by programmed cell death