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

被引：12
作者：
Sun, Zhikun [1 ]
Ma, Xingrong [2 ]
Yang, Hongqi [1 ]
Zhao, Jiahua [1 ]
Zhang, Jiewen [1 ]
机构：
[1] Henan Prov Peoples Hosp, Dept Neurol, Zhengzhou 450003, Henan Province, Peoples R China
[2] Zhengzhou Univ, Affiliated Hosp 1, Dept Neurol, Zhengzhou 450052, Henan Province, Peoples R China
来源：
NEURAL REGENERATION RESEARCH | 2012年 / 7卷 / 05期
关键词：
Alzheimer's disease; apoptosis; beta-amyloid peptide; Bax; brain-derived neurotrophic factor; Bcl-2; tyrosine kinase receptor B; NEURAL STEM-CELLS; ALZHEIMERS-DISEASE; DECREASED LEVELS; PARIETAL CORTEX; BDNF SERUM; PROTEIN; KINASE; DEATH; RECEPTOR;
D O I：
10.3969/j.issn.1673-5374.2012.05.004
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Brain-derived neurotrophic factor was utilized in the present study to treat cell injury models induced by aggregated beta-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 beta-amyloid(25-35)-induced cell activity and the increasing ratio of Bax/BcI-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 beta-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.
引用
收藏
页码：347 / 351
页数：5
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