畜牧兽医学报 ›› 2014, Vol. 45 ›› Issue (9): 1526-1530.doi: 10.11843/j.issn.0366-6964.2014.09.020

• 基础兽医 • 上一篇    下一篇

PrP106-126作用下N2a细胞线粒体的损伤机制

苑方重1,耿梅英1,赵德明2*   

  1. (1.河北农业大学动物医学院,保定 071001;2.中国农业大学动物医学院,国家动物海绵状脑病实验室,北京 100193)
  • 收稿日期:2014-02-13 出版日期:2014-09-23 发布日期:2014-09-23
  • 通讯作者: 赵德明,E-mail:zhaodm@cau.edu.cn
  • 作者简介:苑方重(1977-),男,山东菏泽人,博士,主要从事兽医病理学研究,E-mail:yuanfangzhong@126.com
  • 基金资助:

    国家自然科学基金项目(31172293);高等学校博士学科点专项科研基金(20100008120002)

The Damage Mechanism of Neuroblastoma Cells Mitochondria in the Presence of PrP106-126 Peptide

YUAN Fang-zhong1,GENG Mei-ying1,ZHAO De-ming2*   

  1. (1.College of Veterinary Medicine,Hebei Agricultural University,Baoding 071001,China;2.National Animal Transmissible Spongiform Encephalopathy Laboratory,College of Veterinary  Medicine,China Agricultural University,Beijing 100193,China)
  • Received:2014-02-13 Online:2014-09-23 Published:2014-09-23

摘要:

为探讨Prion相关疾病中神经细胞的损伤机制,应用毒性神经多肽PrP106-126与一定浓度的Fe3+离子共同作用,并通过测定细胞NADH活性评估细胞呼吸链功能状态,检测细胞线粒体膜电位的动态变化,及线粒体内细胞色素C的分布,探讨细胞在PrP106-126与Fe3+共同诱导的氧化应激条件下,N2a细胞线粒体可能的损伤及对整个细胞的影响。试验结果显示,毒性多肽与Fe3+作用下,N2a细胞的NADH酶活性显著下降(P<0.01),降低至正常活性的65%,细胞线粒体膜电位出现明显的去极化(P<0.01),细胞色素C自线粒体释放至细胞质中,并引起pro-caspase-9活化。

Abstract:

 The purpose of this study was to investigate the possible mechanism of neuron cell damage in Prion diseases.And we studied the respiratory chain function of N2a cells by testing the NADH activity after treatment with ferric ions and PrP106-126,as well as the depolarization of the mitochondrial membrane potential and the distribution of cytochrome C.It is proved that the activity of NADH of N2a cells,which were treated with ferric ions and PrP106-126,was significantly decreased (P <0.01) to about 65%.And the mitochondrial membrane potential of N2a cells had been depolarization significantly.It is showed that the cytochrome C were released into cytoplasm and activated the pro-caspase-9.

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