摘要
目的:观察新生大鼠缺氧缺血性脑损伤(HIBD)后海马齿状回增殖细胞分化情况,及碱性成纤维细胞生长因子(bFGF)干预对其的影响,探讨实验大鼠的远期行为学变化。方法:7日龄SD大鼠随机分为假手术组、缺氧缺血组和bFGF干预组,建立HIBD模型(假手术组不予缺氧处理),分别于术后5、10、14、21 d取脑,采用免疫荧光双标记观察大鼠海马齿状回BrdU/MAP-2、BrdU/GFAP阳性细胞表达,并应用Y-迷宫法进行行为学测定。结果:缺氧缺血组及bFGF干预组BrdU/MAP-2、BrdU/GFAP阳性细胞于术后10、14 d较5 d时有所升高(P<0.05),21 d下降至5 d时的水平。与假手术组及缺氧缺血组比较,bFGF干预组于HIBD后各个时间点BrdU/MAP-2、BrdU/GFAP阳性细胞均有所增加(P<0.05)。Y-迷宫测试显示bFGF干预组学习记忆能力较缺氧缺血组有所提高(P<0.05)。结论:HIBD后海马齿状回增殖细胞存在分化为神经元及星形胶质细胞的现象,bFGF能够促进HIBD后海马齿状回增殖细胞向神经元及星形胶质细胞分化,并可以改善大鼠后期行为记忆能力。
Objective To observe the relationship between the hippocampal proliferation and differentiation in dentate gyrus and basic fibroblast growth factor（bFGF） after hypoxic-ischemic brain damage（HIBD） in the neonatal rats and to explore the behavior capability.Methods The neonatal HIBD model was established with 7-day-old rat pups,and randomly divided into the sham group,the hypoxia-ischemia group and the bFGF group.Rats were killed on day 5,10,14 and 21 after operation,respectively.The slices of the brains were undertaken with double immunofluorescence staining to observe the expression of BrdU/MAP-2-positive or BrdU/GFAP-positive cells in dentate gyrus.Y-maze was used for behavior test.Results In the hypoxic-ischemic group and the bFGF group,the expression of BrdU/MAP-2-positive and BrdU/GFAP-positive cells were increased on day 10 and 14 after HIBD when compared with that on day 5（P〈0.05）,and decreased on day 21.In the bFGF group,the expression of BrdU/MAP-2-positive and BrdU/GFAP-positive cells were increased on day 5,10,14 and 21 after HIBD when compared with those in the sham group and the hypoxic-ischemic group（P〈0.05）.In the bFGF group,improvements in behavior and memory were achieved in the hypoxic-ischemic group（P〈0.05）.Conclusions There is neurogenesis in dentate gyrus of hippocampus after HIBD and the cells can propagate and differentiate into the new neurons and astrocytes.The therapy of bFGF promotes cell proliferation and differentiation in dentate gyrus possibly and improves the behavior and memory.It can be concluded that bFGF take part in the mechanism of endogenous neurogenesis after HIBD possibly.
出处
《东南大学学报（医学版）》
CAS
2009年第3期193-197,共5页
Journal of Southeast University(Medical Science Edition)
