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

VernacularTitle: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
Author: Zhi-Kun SUN ¹ ; Jie-Wen ZHANG ; Hong-Qi YANG ; Xing-Rong MA
Author Information

1. 河南省人民医院
Keywords: Brain-derived neurotrophic factor; β-amyloid protein; Apoptosis; Alzheimer's disease
From: Chinese Journal of Neuromedicine 2011;10(1):19-23
CountryChina
Language:Chinese
Abstract: 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.