遗传性癫痫大鼠小脑中p-CaMKⅡ、p-ERK和p-p38蛋白表达的异常变化

The abnormal changes of p-CaMK II, p-ERK and p-p38 proteins in the cerebellum of genetic epileptic rats

目的研究遗传性癫痫大鼠(Tremor,TRM)与正常Wistar大鼠小脑中p-Ca MKII、p-ERK以及pp38蛋白含量的变化,进一步阐明癫痫发病机制。方法应用PCR技术,鉴定基因突变鼠(TRM),确定癫痫阳性大鼠。以Wistar大鼠作为正常对照模型,通过Western blot技术分别测定TRM及Wistar大鼠小脑内p-Ca MKII、pERK以及p-p38的蛋白表达量。结果与正常大鼠相比,TRM大鼠小脑p-Ca MKII蛋白和p-p38蛋白表达量升高,而pERK蛋白表达量没有明显变化。结论 TRM大鼠小脑内p-Ca MKII和p-p38蛋白表达上调,表明Ca MKII与MAPK信号通路可能参与癫痫的发病机制。

Objective To detect the expression changes of p-Ca MKII, p-ERK and p-p38 protein in the cerebellum of genetic epileptic rats（Tremor, TRM） and Wistar rats. Methods TRM rats were identified by PCR technique. The expressions of p-Ca MKII, p-ERK and p-p38 proteins in the cerebellum of TRM rats and Wistar rats were detected by Western blot. Results Compared with the control group, the expression levels of p-Ca MKII protein and p-p38 protein were increased in TRM group; however, there was no significant difference for p-ERK expression between TRM and control groups. Conclusion The overexpressions of p-Ca MKII and p-p38 in the cerebellum of TRM rats indicate that p-Ca MKII and MAPK signal pathways may be involved in the pathogenesis of epilepsy.