BDNF对β-淀粉样蛋白诱导细胞损伤的保护作用  

The effects of brain-derived neurotrophic factor on cell injuries induced by β-amyloid peptide

作　　者：孙治坤[1] 马兴荣[2] 杨红旗[3] 赵建华[1] 马瑜[1] 张杰文[1] 

机构地区：[1]河南省人民医院神经内科,450003 [2]郑州大学第一附属医院神经内科,450002 [3]河南省人民医院老年医学部神经内科,450003

出　　处：《中国神经免疫学和神经病学杂志》2011年第2期87-90,共4页Chinese Journal of Neuroimmunology and Neurology

摘　　要：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。Objective To investigate the effects of brain-derived neurotrophic factor（BDNF） on cell injuries induced by β-amyloid peptide in PC12 cells.Methods Cultured PC12 cells were divided into different groups including different times（0,30 min,1 h,3 h,6 h,12 h,48 h） of 20 μmol/L Aβ25-35 treatment groups,20 μmol/L Aβ25-35 and different concentrations of BDNF（20 ng/mL,50 ng/mL,100 ng/mL） treatment groups,200 nmol/L Trk B receptor inhibitor K252α alone treatment group,20 μmol/L Aβ25-35 and 50 ng/mL BDNF treatment groups,200 nmol/L K252α and 20 μmol/L Aβ25-35 and 50 ng/mL BDNF treatment groups.The viability of PC12 cells and the level of cleaved caspase-3 were detected by MTT and Western blotting,respectively.Results Aβ25-35 treatment could decrease the viability of PC12 cells in a time-depended manner（P0.05）,and increase the expression of cleaved caspase-3.BDNF could significantly prevent the decreased cell viability and the increased expression of cleaved caspase-3 induced by Aβ25-35（P0.05）,and these preventive effects were blocked by Trk B inhibitor K252α（P0.05）.Conclusions BDNF can prevent cell injuries induced by Aβ25-35 by binding to Trk B receptor.

关 键 词：Β-淀粉样蛋白 凋亡 脑源性神经营养因子 阿尔茨海默病 

分 类 号：R742.89[医药卫生—神经病学与精神病学]