中文摘要：

目的观察甘珀酸（生胃酮）对戊四氮点燃大鼠的保护作用和对连接蛋白32的影响.方法观察戊四氮及生胃酮腹腔注射大鼠痫性发作等级及潜伏期的变化,并采用蛋白印迹法测定海马CX32的表达.结果20mg·kg^-1生胃酮组大鼠痫性发作等级较致痫组低,潜伏期明显延长（P＜0.05）;10 mg·kg^-1生胃酮组大鼠痫性发作等级与致痫组无差异,但潜伏期较致痫组显著延长（P＜0.01）.致痫组海马CX32表达较对照组明显增加,20mg·kg^-1生胃酮组与对照组无显著差异.结论反复癫痫发作会诱导CX32异常表达,CX32和缝隙连接参与了癫痫的形成和点燃过程,缝隙连接阻滞剂生胃酮有较明确的抗癫痫作用.

英文摘要：

OBJECTIVE To investigate the effects of carbenoxolone on upregulation of connexin 32（CX32） in the hippocampus of kindled rats. METHODS Before the kindled model was induced by pentylenetetrazole, some rats were administered with carbenoxolone （ 10 mg· kg^-1 or 20 mg· kg^- 1 ）. The hippocampal tissue was used to measure the level of CX32 by western blot technique. REULTS The expression of CX32 was elevated significantly in kindled rats （ P 〈 0.05 ） but was not increased in 20 mg·kg^-1 carbenoxolone treated group as compared with the controls. The seizure stages were not inhibited by 10 mg· kg^-1 carbenoxolone but decreased significantly in 20 mg·kg^- 1 carbenoxolone treated group （P 〈 0.01 ）. The latency in carbenoxolone treated group was prolonged in a dose dependent manner. CONCLUSION The increases of the expression of CX32 might be associated with epilepsy kindling and gap junction blocker. Carbenoxolone plays a certain protective role on seizure development.