摘要
目的建立大鼠颞叶癫痫(temporallo bee pilepsy,TLE)模型,观察大鼠缝隙连接蛋白32(connexin32,CX32)的表达变化,进一步探讨TLE发病机制。方法健康成年雄性Sprague-Dawley大鼠88只,随机为正常对照组(n=8)、手术对照组(n=40)和红藻氨酸(KA)致痫组(n=40),其中手术对照组和KA致痫组又按术后3h、6h、12、24h和7d分为5个亚组,每组8只。通过免疫组织化学染色检测各组CX32蛋白的表达变化。结果KA致痫后3h大鼠的颞叶皮层区及海马区CX32阳性表达逐渐增多,并持续上升,时程越长阳性表达越多,平均光密度值越高(P<0.01)。KA致痫后各时间点CX32平均光密度值明显比对照组增多,差异有显著性(P<0.05);手术对照组与正常对照组相比,CX32平均光密度值差异无显著性(P>0.05)。KA致痫后大鼠颞叶皮层区及海马区均有CX32阳性表达,海马区CX32平均光密度值明显比颞叶皮层高(P<0.05)。结论CX32可能参与颞叶癫痫的发生发展过程,提示CX32特异性的抑制剂有可能为颞叶癫痫的临床治疗开辟新的前景。
【Objective】To observe the expression changes of connexin32 （CX32） in the rat with temporal lobe epilepsy （TLE）, to further explore the pathogenesis of TLE.【Methods】Eighty-eight Sprague-Dawley rats were randomly divided into 3 groups, a control group （n =8）, a operation group （n =40） and a TLE group （n =40）. Established TLE model with Kainic acid, used immunohistochemistry to measure protein of connexin32 at time point of 3 h, 6 h, 12 h, 24 h, 7 d following operation respectively【.Results】The expression of CX32 can be observed in temporal lobe cortex and hippocampus area of the rats induced epilepsy by KA after 3 h, the longer the duration the more positive expression. Furthermore, CX32 positive expression was significantly higher in hippocampus area than in temporal lobe cortex （P 0.05）. Compared with operation group, CX32 expression was significantly higher in TLE group （P 0.05）.【Conclusions】CX32 might play an important role in the pathogenesis of TLE.CX32-specific inhibitors might have clinical treatment of temporal lobe epilepsy
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2010年第5期702-705,共4页
China Journal of Modern Medicine
基金
广西青年科学基金(编号:桂科青0542073)
