【摘要】 目的研究基质相互作用分子1(stromal interaction molecule l,STIM1)在海人酸(Kainic acid,KA)致痫大鼠大脑皮质中的表达变化,探讨其与癫痫发病的关系及意义。方法 48只成年雄性SD大鼠随机分为正常对照组(NS组)24只和海人酸致痫组(KA组)24只,海人酸致痫组给予侧脑室注射KA 2μg/kg(7μl左右)制作KA致痫模型,正常对照组给予侧脑室注射等量生理盐水,观察记录各组大鼠癫痫发作的行为学表现,并于癫痫发作后不同时间点(48h、72h)随机取12只大鼠伤侧皮层脑组织,用半定量RT-PCR、Western blot和免疫组织化学技术检测STIM1的mRNA和蛋白的表达。结果 KA致痫组大鼠于造模后5min左右出现典型痫性发作,达Ⅳ~Ⅴ级,持续数小时;海人酸致痫组STIM1mRNA和蛋白表达水平在各时间点均较对照组显著增高(P<0.05)。结论 STIM1在KA致痫大鼠皮层脑组织中过表达可能参与癫痫的发病机制。更多还原

【Abstract】 Objective To observe the expression change of STIM1 in cortex of rats with seizures induced by kainic acid(KA), and to explore the role of STIM1 in epileptogenesis. Methods Forty eight adult Sprague Dawley(SD) rats were randomly divided into: control group(treated with isotonic Na chloride) and epilepsy group(treated with KA) with 24 in each. The expression of STIM1 mRNA and protein in cortex was detected by RT-PCR and Western blot and immunohistochemistry respectively. Results The epilepsy group showed classical seizure activity(Ⅳ~Ⅴlevel) and last for several hours. The expression levels of STIM1 mRNA and protein in cortex were much higher in epilepsy group than in control group(P<0.05). Conclusion The overexpression of STIM1 in cortex of rats with seizures indicates that STIM1 might be involved in the pathogenesis of epilepsy.更多还原