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目的研究缝隙连接在癫发病机制中的作用。方法以体外培养大鼠海马神经元为研究对象,采用免疫细胞化学方法和实时定量逆转录-聚合酶链反应(RT-PCR)方法观察缝隙连接蛋白(connexin,Cx)32和Cx43的表达,并加用生胃酮干预。结果神经元经无镁液处理1h后Cx32mRNA迅速升高,至5h升高了近10倍;蛋白表达在2h后开始增多(21.80±1.74),8h后(47.30±5.75)较对照组(9.30±1.25)增高了5倍。Cx43水平低于Cx32,无镁液作用5h后mRNA表达显著增多,8h后蛋白表达始明显增强。生胃酮显著抑制了其表达。结论Cx32和Cx43在癫样放电后表达显著增多,生胃酮能够抑制其表达和神经元放电,提示缝隙连接在癫的发生发展过程中具有重要的作用。
Objective To study the role of gap junctions in the pathogenesis of epilepsy. Methods The cultured hippocampal neurons were cultured in vitro and the expressions of connexin (Cx) 32 and Cx43 were detected by immunocytochemistry and real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) Add carbidone intervention. Results Cx32 mRNA in neurons increased rapidly after treated with magnesium solution for 1 hour and increased nearly 10 times after 5 hours. The protein expression began to increase after 21 hours (21.80 ± 1.74), and after 9 hours (47.30 ± 5.75) 1.25) increased by 5 times. After Cx43 was lower than Cx32, mRNA expression increased significantly after 5h without magnesium solution, and protein expression began to increase after 8h. Vivo ketone significantly inhibited its expression. Conclusions Cx32 and Cx43 are significantly increased after epileptiform discharge, and carbenoxolone can inhibit its expression and neuronal discharge, suggesting that gap junction plays an important role in the development of epilepsy.