摘要
目的观察褪黑素(Mel)对癫大鼠海马神经元凋亡及半胱氨酸蛋白酶(caspase)-3表达的影响。方法采用匹罗卡品(Pilo)制作大鼠癫持续状态(SE)模型,随机分为Pilo组、Mel组和对照组,用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法(TUNEL)染色和免疫组化技术检测大鼠海马神经元凋亡数和caspase-3的表达,并与对照组比较。结果SE后6h,Pilo组开始出现少量TUNEL阳性细胞;SE后72h,达到高峰;SE后7d,TUNEL阳性细胞开始减少。SE后6h,Pilo组大鼠海马caspase-3阳性细胞数增多,主要集中于CA1和CA3区;SE后48h,达到高峰;SE后72h,阳性细胞数开始减少;SE后7d,caspase-3表达基本恢复正常。Mel组各时间点大鼠海马TUNEL阳性细胞数和caspase-3表达均明显低于Pilo组大鼠(均P<0.01)。结论Mel可减少癫大鼠海马神经元凋亡,抑制caspase-3的表达,起到神经保护作用。
Objective To observe the effects of Melatonin on hippocampal neuron apoptosis and caspase-3 expression in epileptic rats. Methods Using model of status epilepticus （SE） induced by Pilocarpine, the rats were administered with melatonin （melatonin group ） or saline （Pilocarpine group ） before Pilocarpine injection. The apoptotie neuron was detected by TdT-mediated dUTP Nick End Labeling （TUNEL） and caspase-3 expression was observed by immunocytochemistry method, respectively. Results In Pilocarpine group, the number of TUNEL positive neurons began to increase at 6 h post-SE, peaked at 72 h post-SE, and decreased at 7 d post-SE. Caspase- 3 immunoreactivity began to increase at 6 h post-SE, peaked at 48 h post-SE, especially in CA1 and CA3 region of hippoeampus, began to decrease at 72 h post-SE and dropped to normal level at 7 d post-SE. The numbers of TUNEL positive neurons and caspase-3 expression in Melatonin group were significantly decreased compared to Pilocarpine group at different time points （ all P 〈 0. 01 ）. Conclusion Melatonin plays neuroprotective effect via attenuating hippoeampal neuron apoptosis and inhibiting caspase-3 expression in epileptic rats.
出处
《临床神经病学杂志》
CAS
北大核心
2007年第2期104-107,共4页
Journal of Clinical Neurology
