孙治坤;马兴荣;杨红旗;赵建华;马瑜;张杰文;

• 1:河南省人民医院神经内科
• 2:郑州大学第一附属医院神经内科
• 3:河南省人民医院老年医学部神经内科

摘要(Abstract)：

目的探讨脑源性神经生长因子(brain-derived neurotrophic factor,BDNF)对凝聚态β-淀粉样蛋白25-35片断(Aβ25-35)诱导细胞凋亡的影响。方法采用PC12细胞作为研究对象,将培养的细胞随机分为20μmol/L Aβ25-35处理不同时间组(0、30 min以及1、3、6、124、8 h)、20μmol/L Aβ25-35+不同浓度的BDNF(20、50、100 ng/mL)处理组、单独Trk B受体抑制剂K252α(200 nmol/L)处理组、20μmol/L Aβ25-35+50 ng/mLBDNF处理组、K252α(200 nmol/L)+20μmol/L Aβ25-35+50 ng/mL BDNF处理组。采用MTT法观察不同处理组PC12细胞的活力,采用Western blot法检测不同处理组PC12细胞Cleaved caspase-3表达的变化。结果 20μmol/L的Aβ25-35作用不同时间后细胞活力均明显下降,且呈一定的时间依赖趋势(P<0.05);不同浓度的BDNF(20、501、00 ng/mL)预处理后均可明显抑制20μmol/L的Aβ25-35诱导的细胞活力下降(P<0.05);20μmol/L的Aβ25-35可诱导PC12细胞Cleaved caspase-3表达增高(P<0.05),50 ng/mL的BDNF可明显抑制20μmol/L的Aβ25-35诱导的Cleaved caspase-3表达的增高(P<0.05),Trk B受体抑制剂K252α(200 nmol/L)预处理后,50 ng/mL的BDNF对20μmol/L的Aβ25-35诱导的Cleaved caspase-3表达增高的抑制作用明显减弱(P<0.05)。结论 BDNF对Aβ25-35诱导的细胞损伤具有保护作用,且其保护作用是通过与其特异性受体Trk B结合而实现。

关键词(KeyWords)： β-淀粉样蛋白;凋亡;脑源性神经营养因子;阿尔茨海默病

Abstract:

Keywords:

基金项目(Foundation):

作者(Author): 孙治坤;马兴荣;杨红旗;赵建华;马瑜;张杰文;

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参考文献(References)：

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