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作 者:马玉东[1] 宋岩[1] 张海波[2] MA Yu-dong1, SONG Yan1, ZHANG Hai-bo2(1. Intensive Care Unit, and 2. Department of Neurosurgery, Central Affiliated Hospital of Shenyang Medical College, Shenyang 110024, China)
机构地区:[1]沈阳医学院附属中心医院重症医学科,辽宁沈阳110024 [2]沈阳医学院附属中心医院神经外科,辽宁沈阳110024
出 处:《解剖科学进展》2018年第2期133-135,139,共4页Progress of Anatomical Sciences
基 金:沈阳医学院科技基金项目(20171012)
摘 要:目的神经干细胞移植对脑外伤大鼠神经功能及脑组织Akt表达的影响。方法 108只SD成年大鼠随机分为假手术组(36只)、脑外伤组(36只)和神经干细胞移植组(36只)。采用改良的Feeney氏法制作大鼠脑外伤动物模型,损伤1周后在皮质处局部注射移植神经干细胞,分别在细胞移植后的第7天、14天和21天进行神经功能评分。免疫组织化学方法和Western blot方法检测各组大鼠脑组织Akt与p-Akt蛋白的表达。结果脑外伤组大鼠出现明显的神经功能障碍,神经干细胞移植后第7、14和21天大鼠的神经功能评分明显降低(P<0.05)。与假手术组相比,不同时间点脑外伤组大鼠脑组织Akt与p-Akt蛋白的表达水平显著降低(P<0.05);与相同时间点的脑外伤组大鼠相比,神经干细胞移植组大鼠脑组织的Akt与p-Akt蛋白的表达水平显著升高(P<0.05)。结论神经干细胞移植促进脑外伤大鼠神经功能的恢复可能与上调Akt的表达相关。Objective To study the effect of neural stem cells transplantation on neurological behavior and expression of Akt in rats after traumatic brain injury(TBI). Methods 108 SD rats were randomly divided into: sham group(S, n=36), traumatic brain injury group(TBI, n=36) and neural stem cells transplantation group(N, n=36). TBI model of rats was established by using improved Feeney method. The neural stem cells were transplanted into the damaged cortexes through local injection. Neurological severity scores(NSS) were evaluated on 7th days,14 days and 21th days after cell transplantation, respectively. The expressions of Akt and p-Akt were detected in brain tissues of rats by immunohistochemistry and Western blot. Results The obvious neurobehavioral disorders were observed in TBI group. Compared with the TBI group, the neurobehavioral scores in rats of neural stem cells transplantation group were significantly lower on 7th,14th and 21 days after cells transplantation(P〈0.05). The expression levels of Akt and p-Akt in brain tissues were decreased significantly in TBI group than in sham group, but increased significantly in neural stem cells transplantation group than in TBI group(P〈0.05). Conclusion The neural stem cells transplantation promoting the recovery of brain injury might be related to upregulating the expression of Akt.
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