中文摘要：

目的探讨阻断缝隙连接对大鼠局灶性脑缺血再灌注后海马迟发性神经元死亡（delayed neuronal death，DND）及Bax表达的影响。方法术前2h左侧脑室注射缝隙连接阻断剂甘珀酸（carbenoxolone，CBX），颈内动脉插线法制备大鼠大脑巾动脉缺血模型，采用TUNEL及免疫荧光技术，观察3d后海马DND及Bax表达水平的变化。结果缺血再灌注生理盐水有45％的大鼠出现海马DND；用CBX后仅30％的大鼠出现海马DND，机率明显减小（P〈（0．01）；与假手术组比较，缺血再灌注巾CBX组Bax的表达水平明显增高，但低于缺血再灌注生理盐水（P〈0．01）。结论缝隙连接与局灶性脑缺血再灌注引起的海马DND有密切关系，其原因可能与缺血再灌注后凋亡启动信号南缺血再灌注区通过缝隙连接向远隔部位播散有关，Bax参与了海马神经元凋亡的调节。

英文摘要：

Objective To explore the effect of blocking gap junction communication after focal cerebral ischemia on the delayed neuronal death in ipsilateral hippocampus. Methods A rat model of middle cerebral artery occlusion was made by the intraluminal occlusion technique, carbenoxolone, a gap junction blocker, was used to block gap junction eonmuunication, and the effect of blocking gap junction communication after focal cerebral ischemia on delayed neuronal death in the ipsilateral hippocampus was observed by TUNEL labeling and immunofluorescence staining. Results With no inhibition of gap junction communication, delayed neuronal death was detected in 45% of the animals in hippocampal CAI region 3 days after middle cerebral artery occlusion. With the inhibition of gap junction communication, delayed neuronal death appeared in only 30% of the animals（P〈0. 01）. The expression of Bax gene was significantly lower in the experimental group than that of control group（P〈0. 01）. Conchtsiolts Gap junction communication might be related to delayed neuronal dealh in hippocampus after middle cerebral artery occlusion, and Bax might play an important regulation role in this process.