中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (9): 959-967.doi: 10.4103/1673-5374.133140

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

神经肽 Y 保护大脑皮质神经元作用途径

  

  • 收稿日期:2014-03-05 出版日期:2014-05-20 发布日期:2014-05-20

Neuropeptide Y protects cerebral cortical neurons by regulating microglial immune function

Qijun Li 1, Changzheng Dong 2, Wenling Li 2, Wei Bu 3, Jiang Wu 2, Wenqing Zhao 1, 2   

  1. 1 Graduate School, Hebei Medical University, Shijiazhuang, Hebei Province, China
    2 Department of Functional Neurosurgery, Hebei General Hospital, Shijiazhuang, Hebei Province, China
    3 Department of Neurosurgery, Third Hospital, Hebei Medical University, Shijiazhuang, Hebei Province, China
  • Received:2014-03-05 Online:2014-05-20 Published:2014-05-20
  • Contact: Wenqing Zhao, Graduate School, Hebei Medical University, Shijiazhuang 050017, Hebei Province, China; Department of Functional Neurosurgery, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China, 13832121438@163.com.

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摘要：

神经肽Y可以通过抑制过度激活的大鼠大脑皮质小胶质细胞免疫活性，降低皮质神经元的N-甲基-D-天冬氨酸电流（INMDA），起到保护神经元的作用。实验给予原代培养大鼠皮质小胶质细胞脂多糖处理后，细胞活化水平增高，细胞培养液中白细胞介素1β和肿瘤坏死因子α表达升高，且小胶质细胞中白细胞介素1β和肿瘤坏死因子α的mRNA表达水平也明显增加，用此细胞培养液去孵育原代培养的大鼠皮质神经元后，神经元N-甲基-D-天冬氨酸电流峰值密度明显增高。给予神经肽Y干预后上述作用受到抑制，而加入神经肽Y的Y1受体阻断剂BIBP3226后，神经肽Y的作用完全消失。说明神经肽Y可以降低过度激活的小胶质细胞免疫活性，避免过量生成白细胞介素1β和肿瘤坏死因子a，降低了大鼠大脑皮质神经元N-甲基-D-天冬氨酸电流密度，从而抑制大脑皮质神经元过度兴奋，起到保护神经元的作用。

关键词: 神经再生, 小胶质细胞, 免疫活性, 神经肽Y, 白细胞介素1β, 肿瘤坏死因子α, NMDA电流

Abstract:

Neuropeptide Y has been shown to inhibit the immunological activity of reactive microglia in the rat cerebral cortex, to reduce N-methyl-D-aspartate current (INMDA) in cortical neurons, and protect neurons. In this study, after primary cultured microglia from the cerebral cortex of rats were treated with lipopolysaccharide, interleukin-1β and tumor necrosis factor-α levels in the cell culture medium increased, and mRNA expression of these cytokines also increased. After primary cultured cortical neurons were incubated with the lipopolysaccharide-treated microglial conditioned medium, peak INMDA in neurons increased. These effects of lipopolysaccharide were suppressed by neuropeptide Y. After addition of the neuropeptide Y Y1 receptor antagonist BIBP3226, the effects of neuropeptide Y completely disappeared. These results suggest that neuropeptide Y prevents excessive production of interleukin-1β and tumor necrosis factor-α by inhibiting microglial reactivity. This reduces INMDA in rat cortical neurons, preventing excitotoxicity, thereby protecting neurons.

Key words: nerve regeneration, microglia, immunological activity, neuropeptide Y, interleukin-1β, tumor necrosis factor-α, INMDA, neural regeneration