中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2017, Vol. 12 ›› Issue (7): 1131-1136.doi: 10.4103/1673-5374.211193

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

金钗石斛生物总碱对Aβ25-35诱导大脑皮质神经元损伤的保护

  

  • 收稿日期:2017-04-24 出版日期:2017-07-15 发布日期:2017-07-15
  • 基金资助:

    国家自然科学基金项目（81473201），贵州省教委自然科学基金项目（2010043），贵州省科技基金项目（JZ [2014]2016），贵州省中药现代化项目（[2011]5086）

Protective effects of Dendrobium nobile Lindl. alkaloids on amyloid beta (25–35)-induced neuronal injury

Wei Zhang, Qin Wu, Yan-liu Lu, Qi-hai Gong, Feng Zhang, Jing-shan Shi   

  1. Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou Province, Chin
  • Received:2017-04-24 Online:2017-07-15 Published:2017-07-15
  • Contact: Jing-shan Shi, Ph.D.,shijs@zmc.edu.cn.
  • Supported by:

    This research was financially supported by the National Natural Science Foundation of China, No. 81473201; the Natural Science Foundation of Educational Commission of Guizhou Province of China, No. 2010043; the Science and Technology Foundation of Guizhou Province of China, No. JZ [2014]2016; the Modernization of Traditional Chinese Medicine Project of Guizhou Province of China, No. [2011]5086.

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摘要：

金钗石斛生物总碱是从传统中药石斛中提取的一种生物碱，既往研究显示其具有抗氧化和抗炎作用，且能对氧糖剥夺神经元损伤发挥保护作用，但目前尚不清楚其是否对Aβ诱导的神经元损伤具有保护作用。实验将大鼠大脑皮质神经元以0.025，0.25，2.5 mg/L金钗石斛生物总碱预处理24h，再以10 μM Aβ25-35孵育24h模拟阿尔茨海默病早期阶段损伤。发现金钗石斛生物总碱预处理可以减轻Aβ25-35造成的神经元损伤以及细胞中乳酸脱氢酶的释放过度，同时逆转Aβ25-35诱导的突触前蛋白95 mRNA以及突触素、突触前蛋白95蛋白表达下调。说明金钗石斛生物总碱可以减轻Aβ25-35对神经元的毒性，维持神经突触的完整性，对早期阿尔茨海默病具有神经保护作用。

ORCID:0000-0002-1371-6126(Jing-shan Shi)

关键词: 神经再生, 金钗石斛生物总碱, Aβ, 神经元, 突触, 突触前蛋白95, 认知障碍, 神经保护

Abstract:

Dendrobium nobile Lindl. alkaloids (DNLA), the active ingredients of a traditional Chinese medicine Dendrobium, have been shown to have anti-oxidative effects, anti-inflammatory action, and protective effect on neurons against oxygen-glucose deprivation. However, it is not clear whether DNLA reduces amyloid-beta (Aβ)-induced neuronal injury. In this study, cortical neurons were treated with DNLA at different concentrations (0.025, 0.25, and 2.5 mg/L) for 24 hours, followed by administration of Aβ25–35 (10 μM). Aβ25–35 treatments increased cell injury as determined by the leakage of lactate dehydrogenase, which was accompanied by chromatin condensation and mitochondrial tumefaction. The damage caused by Aβ25–35 on these cellular properties was markedly attenuated when cells were pretreated with DNLA. Treatment with Aβ25–35 down-regulated the expressions of postsynaptic density-95 mRNA and decreased the protein expression of synaptophysin and postsynaptic density-95, all changes were significantly reduced by pretreatment of cells with DNLA. These findings suggest that DNLA reduces the cytotoxicity induced by Aβ25–35 in rat primary cultured neurons. The protective mechanism that DNLA confers on the synaptic integrity of cultured neurons might be mediated, at least in part, through the upregulation of neurogenesis related proteins synaptophysin and postsynaptic density-95.

Key words: nerve regeneration, Dendrobium nobile Lindl. alkaloids, amyloid beta, neurons, synapse, synaptophysin, postsynaptic density-95, cognitive impairment, neuroprotection, neural regeneration