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目的在建立锂-匹罗卡品点燃幼鼠癫模型的基础上,观察各组大鼠行为学改变、各时间点海马缝隙连接蛋白CX32、CX43的表达变化及甘珀酸的干预作用。方法 72只21日龄SD大鼠随机分为对照组(n=24),锂-匹罗卡品致组(n=24),甘珀酸干预组(n=24)。每组按24h、3d、7d、30d时间点又分为4个亚组,每亚组6只。观察大鼠行为变化,并记录大鼠性发作级别,采用免疫组织化学方法分析各组大鼠海马区各时间点CX32、CX43的表达变化。结果锂-匹罗卡品致组大鼠重型样发作(RacineⅣ/Ⅴ级)评分较甘珀酸干预组明显增高(P<0.05),且其潜伏期明显延长(P<0.05);对照组无样发作;海马区CX32在锂-匹罗卡品致后表达增加,3d达高峰,后逐渐下降,至第30天仍高于对照组,与对照组同一时间点比较差异有统计学意义(P<0.05);海马区CX43在锂-匹罗卡品致后表达增加,且随时程延长而增加,与对照组同一时间点比较差异有统计学意义(P<0.05);甘珀酸干预组各组海马区CX32、CX43表达较同一时间点致组降低(P<0.05)。结论 CX32和CX43在样放电后表达显著增多,提示CX32、CX43在癫的发生发展过程中有重要意义;缝隙连接阻断剂甘珀酸具有抗癫作用。
OBJECTIVE: To establish a model of lithium-pilocarpine-ignited neonatal rats with epilepsy, observe the behavioral changes of rats in each group, the changes of the expression of connexin CX32 and CX43 in hippocampus and the effect of carbenic acid in each group. Methods Seventy-two SD rats (21 days old) were randomly divided into control group (n = 24), lithium-pilocarpine group (n = 24), and carbenic acid intervention group (n = 24). Each group according to 24h, 3d, 7d, 30d time point is divided into 4 subgroups, 6 per subgroup. The behavioral changes of rats were observed. The severity of seizure was recorded. The expression of CX32 and CX43 in hippocampus of each group was analyzed by immunohistochemical method. Results In the lithium-pilocarpine group, the Racine Ⅳ / Ⅴ attack score was significantly higher than that in the control group (P <0.05), and the latent period was significantly longer (P <0.05). In the control group The expression of CX32 in hippocampus was increased after lithium-pilocarpine-induced hyperlipidemia, peaked at 3d, then decreased gradually, and still remained higher than the control group on the 30th day, which was statistically different from the control group at the same time point (P <0.05). The expression of CX43 in hippocampus increased with the increase of lithium-pilocarpine, and increased with the prolongation of time course. The difference was significant compared with the control group at the same time point (P <0.05) The expression of CX32 and CX43 in hippocampus of the acid intervention group was lower than that in the same time point (P <0.05). Conclusions The expression of CX32 and CX43 is significantly increased after aspirated discharge, suggesting that CX32 and CX43 are important in the development of epilepsy. Gap junction blocker carbenoxolol has antiepileptic effect.