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作 者:刘志安[1] 樊红彬[2] 徐铁军[1] 王梅申[1]
机构地区:[1]徐州医学院解剖和神经生物学教研室,江苏徐州221002 [2]徐州医学院附属医院神经内科
出 处:《西部医学》2009年第11期1838-1840,1843,共4页Medical Journal of West China
基 金:江苏省教育厅重点实验室开放研究课题(NO:KJS07005)
摘 要:目的探讨短暂性前脑缺血后大鼠海马细胞的死亡形式,为深入研究缺血性脑损伤的机制和脑缺血后治疗时间窗的选择提供形态学依据。方法四动脉阻断法建立大鼠脑缺血(15min)再灌注(0.5h^7d)动物模型、HE染色、TUNEL法原位标记DNA末端和图像分析与统计处理。结果HE染色显示,缺血后24h细胞出现损伤表现,进行性加重,直至缺血后7d。缺血后12h,可见TUNEL阳性细胞,进行性增多,48h增加更为明显,72h达高峰;然后有所减少,但至缺血后7d,依然存在。以上损伤和阳性细胞主要位于海马CA1区。结论短暂性前脑缺血后,细胞坏死和细胞凋亡共同参与了大鼠海马细胞的死亡过程,二者具有相对的一致性且皆主要发生在海马的选择性易损区。Objective To probe into the form of cell death in hippocampus of rat following transient forebrain ischemia. Methods Iscbemia (15min) reperfusion (0.5h-7d) (IR) animal model was created by four artery occlusion (4AO). HE staining, TUNEL staining and image processing and analysis system were used. Results Cell injury was at 24 hours of IR and became worse and worse until the seventh day of postischemia. At 12 hours of postischemia, the TUNEL positive cells were observed. Then the positive cells started to continuously increase. At 48 hours of postischemia increased significantly and at 72 hours to the highest. Then the TUNEL positive cells started to reduce, but at the seventh day of postischemia the apoptosis cells still existed. Conclusion Cell necrosis and cell apoptosis were participated in cell death process in hippocampus of rat following transient forebrain ischemia.
分 类 号:R743.31[医药卫生—神经病学与精神病学]
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