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神经生长因子对新生大鼠缺氧缺血性脑损伤神经细胞凋亡的影响
引用本文:郝红,李宁. 神经生长因子对新生大鼠缺氧缺血性脑损伤神经细胞凋亡的影响[J]. 郑州大学学报(医学版), 2006, 41(5): 909-910
作者姓名:郝红  李宁
作者单位:1. 郑州市第九人民医院药剂科,郑州,450053
2. 河南省肿瘤医院药剂科,郑州,450003
摘    要:目的:探讨神经生长因子(NGF)对新生大鼠缺氧缺血性脑损伤神经细胞凋亡及FasL、Caspase-3表达的影响.方法:新生7 d龄Wistar大鼠54只随机分为3组:假手术组、生理盐水对照组(NS组)和NGF组,每组18只.NS组和NGF组动物制作新生大鼠缺氧缺血动物模型.假手术组只分离左侧颈总动脉后缝合切口,不进行动脉结扎和缺氧处理.NS组和NGF组术后分别腹腔注射生理盐水和NGF.各组分别于模型制作后1 d,3 d,6 d各处死6只动物,取脑组织切片行TUNEL染色检测神经细胞凋亡,同时行免疫组化检测FasL、Caspase-3的表达.结果:NGF组脑组织神经细胞凋亡和FasL、Caspase-3的表达明显低于NS组,但仍高于假手术组,差异均有统计学意义(P<0.05).结论:NGF可抑制新生大鼠缺氧缺血性脑损伤神经细胞的凋亡,其机制可能与其减少FasL和Caspase-3的表达有关.

关 键 词:神经生长因子  缺氧缺血性脑损伤  凋亡  FasL  Caspase-3
收稿时间:2006-01-06
修稿时间:2006-01-06

Effects of NGF on neural cell apoptosis in neonatal hypoxia-ischemia rats
HAO Hong,LI Ning. Effects of NGF on neural cell apoptosis in neonatal hypoxia-ischemia rats[J]. Journal of Zhengzhou University: Med Sci, 2006, 41(5): 909-910
Authors:HAO Hong  LI Ning
Abstract:Aim: To study the effect of NGF on neural cell apoptosis, and expression of FasL and Caspase-3 in neonatal hypoxia-ischemia brain damage (HIBD) rats.Methods: A total of 54 neonatal Wistar rats were randomly allocated into 3 groups: sham operation group, normal saline group and NGF group. The neonatal HIBD model was established in normal saline group and NGF group. In the sham operation group, the left common carotid artery was only separated without ligation. Then the normal saline group and NGF group were injected normal saline and NGF in abdominal cavity, respectively. After 1 d, 3 d and 6 d, the neural cell apoptosis was detected using TUNEL staining, and the expression of FasL and Caspase-3, using immunohistochemistry staining. Results: The apoptosis of neural cells, the expression of FasL and Caspase-3 in the NGF group were significantly lower than those of the normal saline group but higher than those of sham operation group (P<0.05). Conclusion: The protection effect of NGF on HIBD rats may relate to its inhibition of neural cells apoptosis and the expression of FasL and Caspase-3.
Keywords:nerve growth factor  hypoxia-ischemia brain damage  apoptosis  FasL  Caspase-3
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