中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2012, Vol. 7 ›› Issue (12): 896-899.

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

Pine pollen inhibits cell apoptosis-related protein expression in the cerebral cortex of mice with arsenic poisoning

  

  • 收稿日期:2011-11-01 修回日期:2012-02-24 出版日期:2012-04-25 发布日期:2012-04-25

Pine pollen inhibits cell apoptosis-related protein expression in the cerebral cortex of mice with arsenic poisoning

Yanhong Luo1, Yaodong Wei2, Taizhong Wang1, Dongzhu Chen3, Tiansheng Lu3, Ruibo Wu3, Keke Si3   

  1. 1 Department of Clinical Biochemistry and Molecular Biology, Youjiang Medical College for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China
    2 Department of Biochemistry and Molecular Biology, Youjiang Medical College for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China
    3 Grade 2008, Department of Medical Laboratory Science, Youjiang Medical College for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China
  • Received:2011-11-01 Revised:2012-02-24 Online:2012-04-25 Published:2012-04-25
  • Contact: Yaodong Wei, Master, Professor, Department of Biochemistry and Molecular Biology, Youjiang Medical College for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China weiyaodong-555@sohu.com
  • About author:Yanhong Luo★, Master, Associate professor, Department of Clinical Biochemistry and Molecular Biology, Youjiang Medical College for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China

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Abstract:

Previous studies have demonstrated that pine pollen can inhibit cerebral cortical cell apoptosis in mice with arsenic poisoning. The present study sought to detect the influence of pine pollen on apoptosis-related proteins. Immunohistochemistry, western blotting and enzyme-linked immunosorbent assays were used to measure the levels of apoptosis-related proteins in the cerebral cortex of mice with arsenic poisoning. Results indicated that pine pollen suppressed cell apoptosis in the cerebral cortex of arsenic-poisoned mice by reducing Bax, Bcl-2 protein expression and increasing p53 protein expression.