中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2013, Vol. 8 ›› Issue (10): 909-915.doi: 10.3969/j.issn.1673-5374.2013.10.005

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

糖基化终产物-糖基化终产物受体通路引起的大脑皮质神经元损伤

  

  • 收稿日期:2012-12-07 修回日期:2013-02-05 出版日期:2013-04-05 发布日期:2013-04-05

Injury of cortical neurons is caused by the advanced glycation end products-mediated pathway

Ying Xing1, Xu Zhang1, Xiangfu Song2, Zhongwen Lv1, Lingling Hou1, Fei Li1   

  1. 1 China-Japan Union Hospital, Jilin University, Changchun 130033, Jilin Province, China
    2 College of Public Health, Jilin University, Changchun 130021, Jilin Province, China
  • Received:2012-12-07 Revised:2013-02-05 Online:2013-04-05 Published:2013-04-05
  • Contact: Ying Xing☆, M.D., Associate professor, Associate chief physician, Master’s supervisor, China-Japan Union Hospital, Jilin University, Changchun 130033, Jilin Province, China, xingying1970@ 163.com.

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摘要：

糖基化终产物可导致细胞凋亡，可通过增加内质网的应激而导致细胞死亡，其本身也可直接对组织及细胞造成损伤，但其具体损伤机制不明。鉴于此，实验原代培养大鼠大脑皮质神经元，通过不同浓度糖基化终产物(50，100，200，400 mg/L)进行干预培养，并在糖基化终产物作用神经元前后分别加入糖基化产物受体的特异性抗体进行培养。结果显示，随着糖基化终产物的浓度增加，神经元内自由基含量增高，凋亡细胞数量增加，呈剂量依赖性。糖基化终产物作用前后加其受体入特异性抗体可明显减轻皮质神经元的羟自由基和丙二醛含量，并抑制细胞凋亡。说明大脑皮质神经元中糖基化终产物受体抗体可通过拮抗糖基化终产物受体减轻糖基化终产物所致的氧化应激损伤，证实糖基化终产物-糖基化终产物受体通路可能是糖基化终产物致神经元损伤的主要信号通路。

关键词: 神经再生, 糖基化终产物, 糖基化终产物受体, 抗体, 通路, 皮质神经元, 氧化应激, 氧化应激损伤, 凋亡

Abstract:

Advanced glycation end products lead to cell apoptosis, and cause cell death by increasing endoplasmic reticulum stress. Advanced glycation end products alone may also directly cause damage to tissues and cells, but the precise mechanism remains unknown. This study used primary cultures of rat cerebral cortex neurons, and treated cells with different concentrations of glycation end products (50, 100, 200, 400 mg/L), and with an antibody for the receptor of advanced glycation end products before and after treatment with advanced glycation end products. The results showed that with increasing concentrations of glycation end products, free radical content increased in neurons, and the number of apoptotic cells increased in a dose-dependent manner. Before and after treatment of advanced glycation end products, the addition of the antibody against advanced glycation end-products markedly reduced hydroxyl free radicals, malondialdehyde levels, and inhibited cell apoptosis. This result indicated that the antibody for receptor of advanced glycation end-products in neurons from the rat cerebral cortex can reduce glycation end product-induced oxidative stress damage by suppressing glycation end product receptors. Overall, our study confirms that the advanced glycation end products-advanced glycation end products receptor pathway may be the main signaling pathway leading to neuronal damage.

Key words: neural regeneration, brain injury, advanced glycation end products, advanced glycation end products receptor, antibody, pathway, cortical neurons, oxidative stress, oxidative stress injury, apoptosis, neuroregeneration