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

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. Key words: Brain-derived neurotrophic factor;  [3-amyloid protein;  Apoptosis;  Alzheimer＇s disease