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作 者:袁红刚[1] 黄书岚[1] 刘华明[1] 张纯伟[1]
出 处:《中国临床神经外科杂志》2017年第6期419-421,共3页Chinese Journal of Clinical Neurosurgery
摘 要:目的探讨黄芪多糖(APS)对颅脑损伤大鼠学习记忆能力及海马组织脑源性神经生长因子(BDNF)表达的影响。方法将30只成年雄性SD大鼠按随机数字表随机分为3组:假手术组、TBI组、APS组,每组10只。TBI组和APS组建立颅脑损伤大鼠模型,假手术组不建模型。假手术组、TBI组分别给予生理盐水灌胃,APS组给予APS悬液(100 mg/kg)灌胃;每天1次,持续8周。采用Morris水迷宫实验测试大鼠学习记忆能力。水迷宫实验结束后,RT-PCR与Western blot测定海马组织BDNF mRNA和蛋白表达水平。结果与假手术组比较,TBI组大鼠逃避潜伏期明显延长(P<0.05),平台象限路径百分比和平台象限时间明显缩短(P<0.05),海马组织BDNF mRNA和蛋白表达水平明显降低(P<0.05);与TBI组比较,APS组大鼠逃避潜伏期明显缩短(P<0.05)、平台象限路径百分比和平台象限时间明显延长(P<0.05),海马组织BDNF mRNA和蛋白表达水平明显升高(P<0.05)。结论APS能够减轻颅脑损伤所致的大鼠学习记忆能力减退,可能与提高BDNF表达水平有关。Objective To explore effects of astraglaus polysaccharide(APS)on learning and mermory and expression of brain-derived neutrotrophic factor (BDNF) in the hippocampi of rats with traumatic brain injury(TBI). Methods Sixty rats were randomly divided into three groups of 10 animals each3, i.e. sham operation group, ASP group, in which TBI model was established and the rats were treated by oral administration of ASP for 8 weeks and control group, in which TBI model was established and the rats were treated by oral administration of 0.9% saline solution. The learning and memory function were determined by morris water maze after the treatment and then the expression of BDNF protein and mRNA in hippocampal tissues were determined by western-blot and RT-PCR in all the rats. Results The escape latent period was significantly longer platform retention time and platform distance percentage were significantly shorter and the expression of BDNF in the hippocampal tissues was significantly lower in the control group than those in the sham operation group (P〈0.05). The escape latent period was significantly shorter and platform retention time and platform distance percentage were significantly longer and the expression of BDNF in the hippocampal tissues was significantly higher in ASP group than those in the control group (P〈0.05). Conclusion It is suggested that APS can improve learning and memory functions in the rat with TBI and its mechanism may be related to upregulation of the expression of BDNF in the hippocampal tissues.
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