摘要
目的探讨Aβ25-35诱导模拟人类Alzheimer’s病(AD)的大鼠病理模型中神经元受损与老年性记忆减退之间的关系,以及热耐受处理致HSP70产生对其的影响。方法采用海马内一次性注射β-淀粉样多肽25-35片段(Aβ25-35)制作大鼠AD模型,一周后进行水迷宫行为学测定,采用免疫组化法检测海马CA1区HSP70的表达、HE染色观察细胞形态、流式细胞仪检测神经元的坏死和凋亡。结果与对照组相比,海马内注射Aβ25-35后出现学习记忆能力降低,神经元的坏死和凋亡增多,并且海马区有HSP70的生成,而热休克预处理组能够进一步增加HSP70的生成(P<0·05),减轻神经元的坏死和凋亡的程度(P<0·05)。结论海马内注射Aβ25-35诱导的大鼠学习记忆功能低下与凋亡导致神经元数量减少有关,而Aβ的毒性是神经元凋亡的重要原因,热休克预处理通过增加热休克蛋白表达,对神经元起一定的保护作用。
Objective To study the relationship between the neuron loss and the memory deficit induced by β-amyloid peptide fragment 25-35 （Aβ25-35）, and to study the effect of HSP70 production induced by thermtolerance on them. Methods Microinjection of Aβ25-35 into the hippocampus induced the learning and memory dysfunction in rats. On the 8th day the rats were placed into the Morris maze to test intelligence. Then the HSP70 immunohistochemical and HE staining were employed. The flow cytometry （FCM） were used to detect the apoptosis and necrosis of all groups. Results Compared with those Of the controls, learning and memory decreased, apoptotic neurons increased, and HSP70 was expressed in rats injected with Aβ25-35 （P〈0.05）. The HSP70 expression was markedly increased after thermotolerance, and apoptosis was decreased when compared with that of rats injected with Aβ25-35 （P〈0.05）. Conclusion Learning and memory dysfunction in rats induced by Aβ25-35 is related to neuron apoptosis. The cytotoxicity of Aβ25-35 may contribute to the neuron apoptosis. Thermotolerance may have a protective effect on neurons by increasing production of HSP70.
出处
《中国组织化学与细胞化学杂志》
CAS
CSCD
2006年第4期386-391,共6页
Chinese Journal of Histochemistry and Cytochemistry
基金
湖北省自然科学基金资助项目(No.2003ABA170)
关键词
淀粉样蛋白
热耐受
热休克蛋白
凋亡
坏死
Amyloid
Thermotolerance
Heat shock protein
Apoptosis
Necrosis
