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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 neu-ronal 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中动脉缺血模型,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,缺血再灌注中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由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。
Objective To investigate the effect of blocking gap junctions on hippocampal delayed neu-ronal death (DND) and Bax expression following focal cerebral ischemia-reperfusion in rats. Methods The middle cerebral artery occlusion (MCAO) model was made by intracerebroventricular injection of the gap junction blocker carbenoxolone (CBX) and internal carotid artery in rats 2h before surgery. TUNEL and immunofluorescence were used to observe the changes of DND And Bax expression level changes. RESULTS: DND in hippocampus was found in 45% of the rats in ischemia-reperfused saline and in 30% of rats in CBX group. The incidence of DND in hippocampus was significantly decreased (P <0.01). Compared with sham-operation group, The expression of Bax in CBX group was significantly higher than that in ischemia-reperfusion saline group (P <0.01). Conclusions The gap junctions are closely related to the DND induced by focal cerebral ischemia-reperfusion in hippocampus. The reason may be related to the fact that the signal of apoptosis initiating after ischemia-reperfusion is disseminated from the ischemic-reperfusion zone to the distant site through the gap junction, Bax is involved in the regulation of apoptosis in hippocampal neurons.