摘要
目的通过对杏仁核电刺激癫痫模型大鼠脑室内注射c—Jun氨基末端激酶（JNK）特异性抑制剂SP600125，观察海马区的病理变化和JNK水平的变化，探讨SP600125的作用。方法将4JD只Wistar大鼠随机分为4组：空白组、点燃组、加药组和加药对照组各10只，10次癫痫发作后灌注取脑，Westernblot法检测JNK的表达变化，进行尼氏和胶原纤维酸性蛋白（GFAP）染色，各组间进行比较。结果Westernblot显示点燃组海马区的JNK磷酸化水平（0．48±0．04）较空白组（0．38±0．04）和加药组（0．37±0．03）显著增高（P〈0．05），总JNK水平各组之间差异无统计学意义（P〉0．05）。尼氏染色阳性细胞计数加药组（33．41±3．73）较加药对照组（20．10±5．11）显著增高（P〈0．05）。点燃组GFAP阳性细胞计数（65．45±4．53）和加药对照组（67．18±3．52）较空白组（40．37±3．82）和加药组（43．51-±1．83）显著增加（P〈0．05）。结论JNK信号通路可能参与颞叶癫痫海马硬化形成，表现为磷酸化JNK升高，SP600125通过抑制JNK可以缓解海马区病理变化。
Objective By injecting SP600125 into ventricle of amygdale kindled rats, to observe the pathological changes of the hippocampus and the change of C-Jun N-terminal kinase （JNK） phosphoryl- ation, and discuss the action mechanism of SP600125. Methods Forty rats were randomly divided into 4 groups （n = 10 each） ： blank group, kindling group, SP600125 group, DMSO group. Whole-cell extracts of tissues were obtained from the right hippocampus, and Western blotting was used to detect the changes of JNK and phosphorylation of JNK. Pathological changes of the hippocampus and amygdla were observed by GFAP stain and Nissl stain. Results The level of JNK phosphorylation in the hippocampus was significant- ly higher in the kindling group （ 0. 48 ± 0.04 ） than the blank group （ 0. 38 ± 0. 04 ） and the SP600125 group （0.37 ±0.03）. Nissl stain positive cells in the hippocampus of the SP600125 group were signifi- cantly more than those in the the DMSO group （ 20. 10 ± 5. 11 ）. The expression of GFAP in the hippocam- pus of kindling group （65.45 ± 4. 53 ） and DMSO group （ 67. 18 ± 3.52 ） was significantly stronger than that in the blank group （40. 37 ±3.82） and the SP600125 group （43.51 ± 1.83）. Conclusion The role of repeated activation of iNK can be related to the hippocampal sclerosis in these rats. SP600125 had a protective effect on neurons during the kindling procedure.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2012年第7期1352-1354,共3页
Chinese Journal of Experimental Surgery
基金
湖北省自然科学基金资助项目（2009CDB291）
