匹罗卡品致痫大鼠海马calpain活性变化和其对神经元死亡的影响

目的探讨在匹罗卡品致痫的癫痫持续状态（SE）大鼠模型中，钙蛋白酶在大鼠海马组织中的活性，及钙蛋白酶对神经元坏死、凋亡产生的影响。方法雄性成年wistar大鼠，应用匹罗卡品致痫产生SE后60min后终止发作，24h后取材，行HE染色及tunel染色，观察海马神经元的坏死及凋亡情况，以及western blot检测钙蛋白酶1（μ-calpain）的活性。结果癫痫持续状态后24h，海马组织HE染色神经元数量减少，tunel阳性细胞数增加，钙蛋白酶1出现76ku条带。结论大鼠癫痫持续状态后24h，钙蛋白酶1在海马组织神经元活性增加，海马神经元出现坏死及凋亡。钙蛋白酶1与神经元的死亡存在着正相关。

Alterations of Calpain activity in hippocampus of pilocarpine-induced status epilepticus rat and its effect on neuron death

Objective To explore the alterations of u-calpain activity in hippocampus of pilocarpine--induced status epilepticus （SE） rat and its effect on neuron death. Methods The SE model was generated using adult male Wistar rats by piloearpine administration, and that was stopped at 60 min after SE. 24 h after SE, the brain tissues were stained by HE and Tunel, and the neuron necrosis and ap- optosis were observed. The u-ealpain activity was determined by Western blot analysis. Results 24 h after SE, the number of HE stained neurons were decreased. The number of Tunel positive neurons, however, were increased, and the 76 ku cleavage of u-calpain emerged. Conclusions 24h after SE, the activity of u-ealpain, the neuron necrosis and apoptosis were increased in the hippoeampus. The neuron death was correlated with the u-ealpain activity.