中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2018, Vol. 13 ›› Issue (11): 1981-1987.doi: 10.4103/1673-5374.239446

• 原著:退行性病与再生 • 上一篇    下一篇

牛膝多肽保护多巴胺能神经元免受鱼藤酮或6-羟基多巴胺诱导的细胞凋亡

  

  • 收稿日期:2018-06-15 出版日期:2018-11-15 发布日期:2018-11-15
  • 基金资助:

    中国国家自然科学基金项目（81471037, 81770841），江苏省教育厅基础研究项目（14KJA180006），江苏省六大人才高峰项目（SWYY-051），江苏省高等院校领军人才项目

Achyranthes bidentata polypeptide protects dopaminergic neurons from apoptosis induced by rotenone and 6-hydroxydopamine

Su Peng, Li Xu, Jin-Yu Ma, Xiao-Song Gu, Cheng Sun   

  1. Key Laboratory for Neuroregeneration of Jiangsu Province and Ministry of Education, Co-Innovatioin Center of Neuroregeneration, Nantong University, Nantong, Jiangsu Province, China
  • Received:2018-06-15 Online:2018-11-15 Published:2018-11-15
  • Contact: Cheng Sun, PhD,suncheng1975@ntu.edu.cn.
  • Supported by:

    This study was supported by the National Natural Science Foundation of China, No. 81471037, 81770841; a grant from the Basic Research of Jiangsu Education Department of China, No. 14KJA180006; a grant from the Six Talent Summit Project of Jiangsu Province of China, No. SWYY-051; a grant from the Priority Academic Program Development of Jiangsu Higher Education Institutions of China.

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摘要：

既往研究显示牛膝多肽对多种神经元具有神经保护作用，但其是否会抑制有神经毒素引起的细胞凋亡尚不可知。实验设计观察纯化的牛膝多肽组分ABPPk对于多巴胺能神经元凋亡的作用。以ABPPk(25, 50, 100 ng/mL)预处理SH-5YHY和原代多巴胺能神经元12h，然后将细胞暴露于6-羟基多巴胺(50, 150 μM)或鱼藤酮(50, 200 μM)环境36h诱导细胞凋亡。结果显示ABPPk能显著增加SH-SY5Y细胞和原代多巴胺能神经元的存活率，减少培养基中的乳酸脱氢酶活性，减少多巴胺能神经元凋亡数量，提升线粒体膜电位，增加细胞中Bcl2/Bax比例。说明ABPPk可保护多巴胺能神经元免于凋亡，可能有潜力成为治疗多巴胺能神经元丢失相关疾病如帕金森病的有效干预药物。

orcid:0000-0001-8411-4619(Cheng Sun)

关键词: 牛膝多肽, 神经保护, 细胞凋亡, 神经毒素, 线粒体功能障碍, 细胞活性, Bcl2/Bax, 神经再生

Abstract:

It has been well documented that Achyranthes bidentata polypeptides (ABPPs) are potent neuroprotective agents in several types of neurons. However, whether ABPPs protect dopaminergic neurons from apoptosis induced by neurotoxins is still unknown. This study was designed to observe the effect of ABPPk, a purified fraction of ABPPs, on apoptosis of dopaminergic neurons. SH-5YHY cells and primary dopaminergic neurons were pre-treated with ABPPk (25, 50, or 100 ng/mL) for 12 hours. Cells were then exposed to 6-hydroxydopamine (50 or 150 μM) or rotenone (50 or 200 μM) for 36 hours to induce cell apoptosis. Our results demonstrate that ABPPk markedly increased viability in SH-SY5Y cells and primary dopaminergic neurons, decreased lactate dehydrogenase activity and number of apoptotic dopaminergic neurons, elevated mitochondrial membrane potential, and increased Bcl-2/Bax ratio. These findings suggest that ABPPk protects dopaminergic neurons from apoptosis, and that ABPPk treatment might be an effective intervention for treating dopaminergic neuronal loss associated with disorders such as Parkinson’s disease.

Key words: nerve regeneration, Achyranthes bidentata polypeptides, neuroprotection, cell apoptosis, neurotoxin, mitochondrial dysfunction, cell viability, Bcl-2/Bax, neural regeneration