锂-匹鲁卡品致痫大鼠杏仁核神经元损伤及Mg^(2+)的脑保护作用

Mechanisms of lithium-pilocarpine(LPC) induced rat status epilepticus(SE)neuronal necrosis of nucleus amygdalae and the protecting effects of Mg^(2+)

目的:观察锂-匹鲁卡品(LPC)致痫大鼠杏仁核神经元的形态学改变,并观察Mg2+的脑保护作用。方法:选用成年雄性Wistar大鼠75只,并随机分为LPC组、Mg2+组和生理盐水对照组。用LPC诱发癫痫持续状态(SE)3h,在痫性发作终止后第72h将动物处死。将大鼠脑组织制成切片,分别用光镜和电镜观察杏仁核神经元形态学改变。而Mg2+组大鼠在注射匹鲁卡品前腹腔内注射硫酸镁100mg/kg,其余处理同LPC组。结果:两组大鼠在第72h时杏仁核区均出现了嗜酸性神经元,但Mg2+组神经元损伤程度明显低于LPC组。结论:LPC诱导的SE激活了促进程序性细胞死亡的机制,导致杏仁核神经元坏死,而Mg2+对杏仁核神经元具有保护作用。

Objective:To observe the morphology of neuronal necrosis from lithium-pilocarpine(LPC)induced status epilepticus(SE),and to observe the brain protecting effects of Mg 2+ .Methods:SE was induced in adult male Wistar rats with LPC for3hours,and72hours later the rats were killed.We made all rats brain sections to observe the morphology of neuronal necrosis with microscope and electron microscope.The Mg 2+ group were intraperitoneally injected magnesium sulfate before being injected pilocarpine.Results:Seventy two hours after3hours of SE,two groups of rats were found neuronal necrosis in the nucleus amygdalae.But the damage degree of neurons in Mg 2+ group was lower than that of the pilocarpine group.Conclusion:Our results suggested that programmed cell death-promoting mechanisms are activated by SE and induce neuronal necrosis of nucleus amygdalae,and Mg 2+ has protecting effects on the neurons of nucleus amygdalae.