神经干细胞介导P25、P35蛋白表达促进缺血缺氧性脑病新生大鼠神经功能恢复

来源 :2016华南实验动物科学国际研讨会、第三届实验小型猪国际论坛暨广东·九州实验动物学术交流会 | 被引量 : 0次 | 上传用户:yingyingpps
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  目的:探究神经干细胞对缺血缺氧性脑病(hypoxic-ischemic encephalopathy, HIE)新生大鼠的治疗作用及其对P25、P35蛋白表达变化的影响.方法:60只新生7天SD大鼠随机分为3组.SHAM组(假手术组),HIE+PBS组(模型组),HIE+NSC组(治疗组)每组各20只.干细胞治疗后第5、7、14、21天进行神经行为学检测(Rotarod Test旋转实验和Morris水迷宫测试).21天后处死大鼠HE染色观察大鼠病理变化,Western blot检测P35、P25蛋白的表达.结果:Rotarod Test旋转实验结果显示造模后第5天模型组与治疗组大鼠在转轮中坚持时间明显下降,与对照组比较差异有统计学意义(P<0.05);造模后第7、14、21天,模型组与治疗组大鼠在转轮中坚持时间明显升高且治疗组升高趋势明显高于缺血组(P<0.05),第21天模型组与治疗组大鼠在转轮中坚持时间比较差异有统计学意义(P<0.05).Morris水迷宫结果显示3组大鼠的逃避潜伏期随训练天数增加而逐渐缩短,前5天的总体学习成绩的组间差异有统计学意义(P<0.01).第7天开始治疗组时间逐渐缩短,第21天治疗组与缺血组大鼠的逃避潜伏期在各个时间点的差异均有统计学意义(P<0.05).模型组大鼠出现海马区神经元水肿、核染色质结构不清、空泡形成等病理变化,治疗组病理损伤明显减轻.Western blot结果显示与对照组相比缺血组P35表达减少,P25表达增加(P<0.05),而治疗组与缺血组相比较P35表达增多,P25表达减少(P<0.05).结论:神经干细胞可促进大鼠缺血脑损伤后神经功能恢复,可能通过上调P35蛋白表达,下调P25蛋白表达,对脑缺血损伤起保护作用.
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