Neural Regeneration Research ›› 2014, Vol. 9 ›› Issue (9): 959-967.doi: 10.4103/1673-5374.133140

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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.

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