脑源性神经生长因子通过调节Bax/Bcl表达抑制β-淀粉样蛋白诱导的细胞凋亡  

BDNF inhibits β-amyloid protein-induced cell apoptosis by regulating Bax/Bcl expressions

作　　者：孙治坤[1] 张杰文[1] 杨红旗[2] 马兴荣[3] 

机构地区：[1]河南省人民医院神经内科,郑州450003 [2]老年医学部神经内科 [3]郑州大学第一附属医院神经内科,郑州450052

出　　处：《中华神经医学杂志》2011年第1期19-23,共5页Chinese Journal of Neuromedicine

摘　　要：目的 探讨BDNF对凝聚态β-淀粉样蛋白25-35片断（Aβ25-35）诱导细胞损伤特别是凋亡的影响.方法 MTT法观察细胞活力,Annexin V-PI双染色法观察细胞凋亡,Western blotting法检测Bax及Bcl-2表达,应用Trk B受体抑制剂K252a（200 nmol/L）观察50 ng/mL BDNF对20 μmol/L的Aβ25-35诱导细胞损伤的抑制作用机制.结果 MTT检测结果及Annexin V-PI双染色法发现50ng/mL的BDNF预处理可显著地抑制20μmol/L的Aβ25-35诱导的PC12细胞活力的下降及细胞凋亡;Western blotting检测发现50 ng/mL的BDNF对20μmol/L的Aβ25-35诱导的PC12细胞Bax表达升高、Bcl-2表达降低及Bax/Bcl-2比值上调均有明显的抑制作用,该作用可被Trk B受体抑制剂K252a（200 nmol/L）抑制.结论 BDNF对Aβ25-35诱导的细胞损伤特别是细胞凋亡具有保护作用,该保护作用是通过与其特异性受体Trk B结合实现的.Objective To investigate the effect of BDNF on cell injuries, cell apoptosis especially, induced by 25-35 segment of β-amyloid protein （Aβ25-35） at condensed state in PC12 cells.Methods The viability of PC12 cells, the apoptosis of PC12 cells and the expressions of Bax and Bcl-2 were detected by MTT, Annexin V-PI staining and Western blotting, respectively. Trk B receptor inhibitor K252a （200 nmol/l） was employed to observe the mechanism of 50 ng/ml BDNF on Aβ25-35 （20 μmol/L）-induced cell injury. Results BDNF （50 ng/ml） could significantly prevent the decrease of cell viability and cell apoptosis, and the increase of Bax expression and the decrease of Bcl-2 expression induced by 20 μmol/L Aβ25-35, and prevent the increase of up-regulation of Bax/Bcl-2 ratio; and these effects were blocked by K252a （200 nmol/1）. Conclusion BDNF can prevent Aβ25-35-induced cell injury, cell apoptosis especially, by binding to its specific receptor Trk B.

关 键 词：脑源性神经营养因子 淀粉样蛋白 细胞凋亡 阿尔茨海默病 

分 类 号：R749.16[医药卫生—神经病学与精神病学]