摘要
目的 探讨碱性成纤维细胞生长因子 (bFGF)对红藻氨酸损毁Meynert基底核造成的阿尔茨海默病 (AD)模型大鼠室管膜下层及海马齿状回神经细胞增殖的影响。方法 AD处理组及AD对照组大鼠前脑Meynert基底核注射红藻氨酸制造阿尔茨海默病模型 ;正常对照组注射生理盐水。AD处理组造模后每天侧脑室注射bFGF共 7d ;AD对照组及正常对照组同时间注射生理盐水。BrdU标记增殖细胞。TUNEL方法标记DNA片段 ,原位检测凋亡细胞。计数室管膜下层和海马齿状回BrdU阳性细胞与凋亡细胞数。结果 AD处理组大鼠与AD对照组大鼠相比 ,室管膜下区及海马齿状回BrdU阳性细胞明显增加 (P <0 0 1) ,而凋亡细胞无明显差异 (P >0 0 5 )。AD对照组大鼠与正常对照组大鼠相比 ,室管膜下区与海马齿状回BrdU阳性细胞数及凋亡细胞均没明显差别 (P >0 0 5 )。结论 bFGF可促进AD模型大鼠脑内神经细胞的增殖 。
Objective To study the effect of basic fibroblast growth factor on neurogenesis in brain of rat Alzhermer disease(AD) model with NBM lesion induced by kainic acid. Methods AD model was established by inducing through leisioning NBM lesions with kainic acid. AD rats received bFGF or saline infusion into the cerebroventricular space daily after the induction of AP. After 7 days bFGF infusion, 5-BrdU was used to label the neural progenitors and the survival of newborn cells after bFGF infusion. TUNEL was used to label the apoptotic cell. Positive cells labeled for 5-BrdU or TUNEL in the subventicular zone and the dentate gyrus were counted.Results When compared to AD group, the number of 5-BrdU positive cells in bFGF treatment group significantly increased. But the number of TUNEL positive cells was not significantly different from that of the AD group. The number of 5-BrdU positive cells and the number of TUNEL positive cells was not significantly different from that of the nomal control group.Conclusion bFGF can acceleration the proliferation of neural progenitors in the subventicular zone and the dentate gyrus in AD rat.
出处
《广东医学》
CAS
CSCD
2003年第4期366-368,共3页
Guangdong Medical Journal
