大鼠内侧隔区预损毁对海马迟发性神经元死亡的影响

Experimental study on the effect of MS lesion on delayed neuronal death in hippocampus after cerebral ischemia-reperfusion

目的 :探讨乙酰胆碱 (ACh)对短暂性全脑缺血再灌后海马迟发性神经元死亡 (DND)的作用。方法 :80只健康雄性Wistar大鼠随机分为 5组。Ⅰ组 :手术对照组 ;Ⅱ组 :单纯内侧隔区 (MS)损毁组 ;Ⅲ组 :单纯脑缺血再灌注组 ;Ⅳ组 :MS假性损毁脑缺血再灌注组 ;Ⅴ组 :MS预损毁脑缺血再灌注组 ,动物先行MS损毁 ,第 15d再行血管阻断 ,使脑缺血 2 0min ,并于恢复灌注 72h后处死 ,将脑采用常规石蜡包埋、切片 ,Nissle、HE和Tunel免疫组化染色 ,在光镜下观测计数海马的神经元数。结果 :①DND细胞主要发生在各缺血再灌注组 (Ⅲ、Ⅳ、Ⅴ组 )的海马CA1区 ,其他各区未发现明显变化 ;②Ⅴ组较Ⅲ、Ⅳ组DND明显减轻 ,差异有统计学意义 (P <0 .0 5 )。结论 :ACh参与短暂性全脑缺血再灌后海马CA1区迟发性神经元损伤过程 。

Aim: To study the effects of acetylcholine (ACh) on the delayed neuronal death (DND) of hippocampal neurons after transient cerebral ischemia reperfusion. Methods: A total of 80 rats were allocated into 5 groups at random.Group I, contrast group only being operated on (but not suffering the lesion of medial septum (MS)); Group Ⅱ, only suffering the lesion of MS; Group Ⅲ, the cerebral ischemia reperfusion group; Group Ⅳ, the cerebral ischemia referfusion with shamed lesion of medial septum; Group Ⅴ, the cerebral ischemia referfusion with the lesion of medial septum in advance. In Group Ⅴ,the rats were firstly suffered the lesion of medial septum, then recovered for 15 days.Secondly they were subjected to the 4 vessel occlusion for 20 minutes and reperfused for 72 hours and executed finally. The brains were regularly embedded by paraffin wax,sectioned and stained by Nissle staining, HE staining and Tunel immunohistochemical staining. The hippocampal neurons were counted and evaluated under light microscope. Results: ①The DND occurred only in CA1 regions of groups with the cerebral ischemia and reperfusion (Group Ⅲ,Ⅳ,and Ⅴ), no obvious changes were observed in other regions of hippocampi. ②Compared with Group Ⅲ and Ⅳ,the lesion of the labeled DND neurons of group Ⅴ was obviously alleviated, the difference was significant ( P <0.05). Conclusion: Acetylcholine participates in lesion during the delayed neuronal death in CA1 subfield of hippocampi.The lesion of MS could alleviate the damage of CA1 neurons after ischemia.