Neural Regeneration Research ›› 2012, Vol. 7 ›› Issue (5): 347-351.

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Brain-derived neurotrophic factor prevents beta- amyloid-induced apoptosis of pheochromocytoma cells by regulating Bax/Bcl-2 expression

Zhikun Sun1, Xingrong Ma2, Hongqi Yang1, Jiahua Zhao1, Jiewen Zhang1   

  1. 1 Department of Neurology, Henan Provincial People’s Hospital, Zhengzhou 450003, Henan Province, China
    2 Department of Neurology, the First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, Henan Province, China
  • Received:2011-09-24 Revised:2011-12-22 Online:2012-02-15 Published:2012-02-15
  • Contact: Jiewen Zhang, Doctor, Chief physician, Department of Neurology, Henan Provincial People’s Hospital, Zhengzhou 450003, Henan Province, China zhangjiewen9900@126.com
  • About author:Zhikun Sun☆, Doctor, Attending physician, Department of Neurology, Henan Provincial People’s Hospital, Zhengzhou 450003, Henan Province, China Zhikun Sun and Xingrong Ma contributed equally to this work.

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Abstract:

Brain-derived neurotrophic factor was utilized in the present study to treat cell injury models induced by aggregated β-amyloid(25-35). Methylthiazolyldiphenyl-tetrazolium bromide assay and western blot analysis showed that brain-derived neurotrophic factor provided neuroprotection against cellular apoptosis by suppressing the decline in β-amyloid(25-35)-induced cell activity and the increasing ratio of Bax/Bcl-2. After treating pheochromocytoma cells with tyrosine kinase receptor B receptor inhibitor K252a, brain-derived neurotrophic factor reverses the above- mentioned changes. The experimental findings suggested that brain-derived neurotrophic factor prevented β-amyloid peptide-induced cellular apoptosis by modulating Bax/Bcl-2 expression, and this effect was associated with binding to the specific tyrosine kinase receptor B receptor.

Key words: Alzheimer’s disease, apoptosis, β-amyloid peptide, Bax, brain-derived neurotrophic factor, Bcl-2, tyrosine kinase receptor B