摘要
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。
Objective To clarify if programmed cell death mechanisms induced by seizures take part in the necrotic process of neurons.Methods Seizure was induced by pilocarpine (P) in Sprague Dawley adult rats which were allowed to recover for 24 or 72 hours before perfusion fixation. Neuronal death was assessed by light microscopy with the hematoxylin eosin (HE) staining and with in situ terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). Bax and Bcl 2 protein expression were examined by histochemistry. Results Twenty four and 72 hours after seizures, neuronal death in hippocampus CA1 region was morphologically necrotic. TUNEL positive and morphologically necrotic cells increased in the hippocampal CA1 region at 72 hours after seizures,there was significant difference compared with controls ( P <0.001). Bax expression was also increased in the hippocampal CA1 region at 72 hours after seizures ( P <0.001), but Bcl 2 expression did not increase, while Bcl 2/Bax ratio decreased. Conclusion Seizures induced late onset neuronal necrosis was accompanied by programmed cell death mechanisms.
出处
《中华儿科杂志》
CAS
CSCD
北大核心
2003年第4期290-292,T003,共4页
Chinese Journal of Pediatrics
