表没食子儿茶素没食子酸酯对癫痫大鼠学习记忆能力的影响及其作用机制  

Effect and Mechanism of Epigallocatechin-3-gallate on Learning and Memory Abilities of Epileptic Rats

作　　者：谢涛[1] 和学欣 孙倩[1] 毛卓锋[1] 王晓鹏[1] XIE Tao;HE Xuexin;SUN Qian;MAO Zhuofeng;WANG Xiaopeng(The Second Hospital of Hebei Medical University,Shijiazhuang 050000,China;Shijiazhuang Hospital of Traditional Chinese Medicine,Shijiazhuang 050000,China)

机构地区：[1]河北医科大学第二医院,石家庄050000 [2]石家庄市中医院,石家庄050000

出　　处：《中国实验方剂学杂志》2024年第8期34-40,共7页Chinese Journal of Experimental Traditional Medical Formulae

基　　金：国家自然科学基金项目(81671292);河北省中医药管理局项目(2023326)。

摘　　要：目的:探讨表没食子儿茶素没食子酸酯(EGCG)对杏仁核电点燃癫痫大鼠学习记忆能力的影响,探讨其作用机制。方法:雄性SD大鼠随机分为正常组、模型组、干预组(模型+25 mg·kg^(-1)EGCG)、EGCG组(25 mg·kg^(-1)EGCG)。EGCG组大鼠仅给予EGCG腹腔注射,正常组大鼠仅给予电极植入,另外各组给予杏仁核电刺激制备慢性点燃癫痫模型。EGCG每日于电刺激前给予腹腔注射,在最后1次电刺激24 h,应用Morris水迷宫记录大鼠逃避潜伏期,目标象限百分比;行为学测试结束后24 h,各组大鼠断头处死,尼氏染色观察海马神经元数量;应用透射电镜(TEM)观察海马突触致密物厚度、突触间隙、活动带长度及突触界面曲率;通过蛋白免疫印迹法(Western blot)检测海马突触相关蛋白:突触囊泡蛋白(Syt)、突触后致密蛋白-95(PSD-95)、Kalirin-7表达情况。结果:与正常组比较,模型组大鼠逃避潜伏期明显延长(P<0.05,P<0.01),目标象限比明显降低(P<0.05);海马神经元数量显著减少(P<0.01);大鼠海马突触间隙明显增宽、活性带长度、突触后致密物厚度明显减低(P<0.05,P<0.01);海马突触相关蛋白Syt、PSD-95、Kalirin-7蛋白表达明显降低(P<0.05,P<0.01)。与模型组比较,干预组大鼠逃避潜伏期明显缩短(P<0.05,P<0.01),目标象限百分比明显提高(P<0.05);海马神经元数量显著增加(P<0.01);大鼠海马突触间隙明显缩短、活性带长度、突触后致密物厚度明显增加(P<0.05,P<0.01);大鼠突触相关蛋白Syt、PSD-95、Kalirin-7表达明显升高(P<0.05,P<0.01)。结论:EGCG可有效改善癫痫大鼠认知功能,其保护作用可能是通过保护海马突触超微结构及调节突触相关蛋白Syt、PSD-95、Kalirin-7表达来实现的。Objective:To investigate the effects of epigallocatechin-3-gallate(EGCG)on learning and memory abilities of amygdala electrical kindling-induced epilepsy in rats and its mechanism.Method:Male SD rats were randomly divided into the normal group,model group,intervention group(model+25 mg·kg^(-1) EGCG),and EGCG group(25 mg·kg^(-1) EGCG).Rats in the EGCG group were only given EGCG intraperitoneal injection,those in the normal group were only given electrode implantation,and those in the other experimental groups were given amygdala electrical kindling stimulation to establish a chronic kindling epilepsy model.EGCG was injected intraperitoneally daily before electrical stimulation.Twenty-four hours after the last electrical stimulation,the escape latency and percentage of target quadrant were recorded by the Morris water maze.Twenty-four hours after the behavioral test,rats in each group were sacrificed by decapitation.The number of hippocampal neurons was observed by Nissl staining.The thickness of postsynaptic density in the hippocampus,synaptic cleft,length of active zone and the curvature of synaptic interface were observed by transmission electron microscopy(TEM).The expressions of synapse-related proteins synaptotagmin(Syt),postsynaptic density-95(PSD-95)and Kalirin-7 in the hippocampus were examined by Western blot.Result:Compared with those in the normal group,the escape latency was significantly prolonged(P<0.05,P<0.01)and the target quadrant ratio was significantly decreased in the model group(P<0.05).The number of hippocampus neurons decreased significantly(P<0.01).The synaptic cleft of the hippocampus was widened significantly,and the length of active zone and the thickness of postsynaptic density were significantly decreased(P<0.05,P<0.01).The expressions of synapse-related proteins Syt,PSD-95 and Kalirin-7 in the hippocampus were significantly decreased(P<0.05,P<0.01).Compared with those in the model group,the escape latency was significantly shortened and the percentage of target quadrant was signific

关 键 词：杏仁核点燃 癫痫 表没食子儿茶素没食子酸酯 认知 海马超微结构 

分 类 号：R2-0[医药卫生—中医学] R22R242R285.5R742.1