bFGF与痴呆及其神经细胞凋亡基因的实验研究

Alzhermer's disease is a senile disease of central nerve system. Owing to the number of aged people is increasing quickly in the world, AD has became or will become severe social trouble. It is very important to study AD's pathogenesis and treatment. The in vitro and in vivo AD model were established usingβ25－35 amynoid peptide in the study. The cell apoptosis and protain express level of apoptosis related gene Bcl-2/Bax/ICE were determined in basal forebrain and hippocampal formation, and the effect of basic fibroblast growth factor(bFGF) on the in vitro and in vivo AD model was studied. The result showed that the in vitro and in vivo AD model were established successfully using β25－35 amynoid peptide. β25－35 amynoid peptide induced cells apoptosis with special morphological change and ladder-shaped DNA electrophoretic pattern in vitro and in vivo and destroyed learning and memory in vivo.The level of Bcl-2 protain expression is less than Bax in Western blot. bFGF with different doses could siginificantly reduce the rate of apoptosis(resist or improve apoptosis), and increase the level of Bcl-2 protain expression and reduce the level of Bax/ICE protain expression, and improve learning and memory in vivo. The results indicated that bFGF could inhibit the cell apotosis in basal forebrain and hippocampal formation caused byβ25－35 amynoid peptide, and improve the learning and memory in rats with AD. The study provided new idea and experimental basis for AD's treatment.

由β25-35淀粉样肽神经毒作用建立离体和在体大鼠AD型痴呆模型，研究基底前脑和海马结股窬赴蛲觥⒌蛲鱿喙鼗騝aspases和Bcl-2及其蛋白表达，以及bFGF的调控作用，进一步探讨老年痴呆的发病机理，并为老年痴呆治疗措施的寻求提供新的和有力的实验依据。

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