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- W3028709097 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.Key words: Brain-derived neurotrophic factor; [3-amyloid protein; Apoptosis; Alzheimer＇s disease" @default.
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- W3028709097 date "2011-01-15" @default.
- W3028709097 modified "2023-09-25" @default.
- W3028709097 title "BDNF inhibits β-amyloid protein-induced cell apoptosis by regulating Bax/Bcl expressions" @default.
- W3028709097 doi "https://doi.org/10.3760/cma.j.issn.1671-8925.2011.01.005" @default.
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