摘要
目的探讨GM1对局灶性脑缺血再灌注后神经元凋亡作用的机制。方法运用双肾双夹法建立肾血管性高血压大鼠模型,采用线栓法制备高血压大鼠短暂性局灶性脑缺血再灌注模型,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至24 h在缺血区皮质XRCC1表达出现显著减低(P<0.05);再灌注24h缺血区皮质神经细胞发生凋亡,神经细胞XRCC1的表达强度与凋亡呈负相关。GM1治疗后缺血区皮质XRCC1的表达显著升高,凋亡显著减少(P<0.05)。结论GM1通过提高肾血管性高血压大鼠局灶性脑缺血再灌注后神经细胞XRCC1的表达,发挥了抗神经细胞凋亡的作用。
Objective To explore the mechanism of GM1 on neuronal apoptosis after focal cerebral ischemia/reperfusion. Methods XRCC1 was detected at 3h,6h, 12h ,24h after cerebral ischemia/reperfusion in renovascular hypertensive rats with immunohistochemistry, DNA fragmentation was detected at 24h after cerebral isehemia/reperfusion with TUNEL. Results The grey value of XRCC1 increased significantly in the isehemic cortex as early as 3 hours after reperfusion and remained increased until 24 hours after reperfusion in operating group （ P 〈 0. 05 ）, however, it decreased at the same time in same area after reperfusion in GM1 group（ P 〈 0.05） ; there were no TUNEL postive cells at isehemic cortex in shame - operating group and plenty of TUNEL postive cells at the same area in operating group ; GM1 reduced TUNEL postive cells significantly （ P 〈 0. 05 ）. Conclusion GM1 can reduced neuronal apoptosis after cerebral ischemia/reperfusion in renovaseular hypertensive rats by increased DNA repair proteins XRCC1.
出处
《中国实用神经疾病杂志》
2006年第1期2-4,共3页
Chinese Journal of Practical Nervous Diseases
