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目的动态观察锂-匹罗卡品诱导的皮质发育不良(Cortical dysplasia,CD)大鼠痫性发作后海马区谷胱甘肽-硫转移酶-π(GST-π)的表达,探讨GST-π在CD所致癫痫中耐药的可能机制。方法在SD大鼠孕17d腹腔内注入卡莫司汀(BCNU)制作CD大鼠模型,锂-匹罗卡品诱导CD大鼠痫性发作,应用免疫组化观察致痫后急性期、静止期和慢性期GST-π在海马区的表达。结果与正常对照组比较,GST-π在CD组大鼠海马的明显表达增高(P<0.05);与CD组比较,GST-π在CD癫痫组大鼠海马区的表达在致痫后3h、24h和3d差异无统计学意义(P>0.05),15d时逐渐增加,并于60d时达到高峰(P<0.01～0.05)。结论GST-π的高度表达是CD大鼠慢性期内癫痫反复发作并产生耐药的可能机制之一。
Objective To observe the expression of glutathione S-transferase-π (GST-π) in hippocampus of rats with lithium-pilocarpine-induced cortical dysplasia (CD) Possible Mechanism of Drug Resistance in Epilepsy Induced by. Methods CD rat model was established by intraperitoneal injection of carmustine (BCNU) on the 17th day of SD rats, and epileptic seizures were induced by lithium-pilocarpine. The acute and quiescent phase of epilepsy was observed by immunohistochemistry And chronic GST-π expression in the hippocampus. Results Compared with the normal control group, the expression of GST-π was significantly increased in the hippocampus of the CD group (P <0.05). Compared with the CD group, the expression of GST-π in the hippocampus of the CD epileptic group was significantly increased There was no significant difference between 24h and 3d (P> 0.05), and gradually increased on the 15th day, reaching the peak on the 60th day (P <0.01 ~ 0.05). Conclusion The high expression of GST-π is one of the possible mechanisms of recurrent seizures and drug resistance in chronic phase of CD rats.