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机构地区:[1]南京医科大学附属南京第一医院神经内科,南京210006 [2]郑州大学第二附属医院神经内科,郑州450003
出 处:《神经病学与神经康复学杂志》2006年第3期166-169,190,共5页Journal of Neurology and Neurorehabilitation
摘 要:目的从 DNA 损伤和修复的角度探讨局灶性脑缺血再灌注后神经元凋亡的机制。方法运用双肾双夹法建立肾血管性高血压大鼠模型,采用四血管法制备高血压大鼠全脑缺血再灌注模型,免疫组化法检测再灌注过程中鼠脑 DNA 损伤修复,蛋白 XRCC1、TUNEL 法检测凋亡。结果与假手术组相比,脑缺血再灌注3h 在缺血区皮质和海马 CA1区 XRCC1表达出现显著减低,这种减低一直持续到缺血再灌注24h(P<0.05);再灌注24h 缺血区皮质和海马 CA1区神经细胞发生了凋亡,神经细胞XRCC1的表达强度与凋亡呈负相关。结论脑缺血再灌注早期神经细胞 XRCC1表达的减少可能导致机体对此时出现的 DNA单链断裂修复的能力下降,造成了再灌注后期发生了凋亡。Objective to explore the relationship between the expression of DNA repair protein XRCC1 and DNA fragmentation in neuronal cell after focal ischemia/reperfusion of renovascular hypertensive rats.Methods XRCC1 is detected at 3h,6h,12h,24h after cerebral ischemia/reperfusion with immunohistochemistry;DNA frag- mentation is detected at 24h after cerebral ischemia/reperfusion with TUNEL.Results The grey value of XRCC1 was increased significantly in the ischemic cortex and the CA1 region of hippocampus as early as 3 hours after reper- fusion and remained increased until 24 hours after reperfusion in the operating group(P<0.05);there was no posi- tive cell at ischemic cortex and the CA1 region of hippocampus in the operating group.There were plenty of positive cells at the same area in the shame-operating group and there was a significantly negative correlation between the ex- pression of XRCC1 and the occurrence of DNA fragmentation. Conclusion XRCC1 begins to reduce at the early period and maintained reduced until the late period of ischemia/reperfusion in RHR.It may contribute at least partial- ly to DNA fragmentation at the late period of focal cerebral ischemia/reperfusion.
分 类 号:R544.1[医药卫生—心血管疾病]
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