CAJ | 학술논문

目的研究大鼠杏仁核电点燃癫痫模型海马中JNK的磷酸化改变,探讨JNK磷酸化与癫痫发生发展的关系.方法建立大鼠杏仁核电点燃癫痫模型.设立空白对照组、手术对照组、点燃组,癫痫点燃成功后取脑,分别采用Western blot和免疫荧光方法检测海马中JNK的表达变化,采用TUNEL染色和GFAP免疫组化染色观察海马形态学改变.结果 36只大鼠在12-20 d成功点燃.Western blot显示点燃组磷酸化JNK水平较手术对照组和空白对照组高(P<0.05).形态学检测显示点燃组海马区神经元缺失及神经胶质细胞增生(P<0.05).结论电刺激诱发大鼠癫痫发作后,海马组织JNK磷酸化水平升高,该信号通路的激活可能参与颞叶内侧癫痫海马硬化的发生过程.
목적 연구대서행인핵전점연전간모형해마중JNK적린산화개변,탐토JNK린산화여전간발생발전적관계.방법 건립대서행인핵전점연전간모형.설립공백대조조、수술대조조、점연조,전간점연성공후취뇌,분별채용Western blot화면역형광방법 검측해마중JNK적표체변화,채용TUNEL염색화GFAP면역조화염색관찰해마형태학개변.결과 36지대서재12-20 d성공점연.Western blot현시점연조린산화JNK수평교수술대조조화공백대조조고(P<0.05).형태학검측현시점연조해마구신경원결실급신경효질세포증생(P<0.05).결론 전자격유발대서전간발작후,해마조직JNK린산화수평승고,해신호통로적격활가능삼여섭협내측전간해마경화적발생과정.
Objective To investigate the change of phosphorylation of JNK in the hippocampus of epilepsy rats kindled by chronic electrical stimulation in the basolateral nucleus of the amygdala. Method Eighty male Wistar rats were randomly divided into 3 groups:15 in blank control group,15 in sharn group and 50 in kindling group.The amygdala of the rats in the kindling group was stimulated with constant pulse current. Rats'seizures and electroencephalogram were recorded throughout the stimulation process.JNK phosphorylation level in the rat hippocampus was detected by Western blot. TUNEL staining and immunohistochemical staining of GFAP were performed to evaluate the neuronal death and gliosis in the hippocampus. Results Thirty-six rats were kindled successfully 12 to 20 days after the kindling began.The level of JNK phosphorylafion in the hippocmnpns was significantly higher in kindled rats(2.39±0.14)than those in other two groups(1.13±0.06 in the sham group,1.11±0.77in control group)(P<0.05).There was no significant difference in JNK phosphorylation between the sham group and the control group(P>0.05).Expression of GFAP in the hippocampus of kindled rats was significantly stronger than those in the blank control group and in the sham group(P<0.05).TUNEL staining positive cells in the hippocampus of kindled rats were significantly more than those in the blank control group and in the sham group(P<0.05).Conclusions The level of JNK phosphorylation in the hippocampns increases in the amygdala kindled rats.JNK signal transductiou pathway may be involved in the process of hippocampal sclerosis in the mesial temporal lobe epilepsy.