Open Access

α7 nicotinic acetylcholine receptor agonist inhibits the damage of rat hippocampal neurons by TLR4/Myd88/NF‑κB signaling pathway during cardiopulmonary bypass

  • Authors:
    • Keyan Chen
    • Yingjie Sun
    • Yugang Diao
    • Liu Ji
    • Dandan Song
    • Tiezheng Zhang
  • View Affiliations

  • Published online on: August 4, 2017     https://doi.org/10.3892/mmr.2017.7166
  • Pages: 4770-4776
  • Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The present study aimed to investigate the effect of α7 nicotinic acetylcholine receptor (α7nAChR) agonist on the damage of hippocampal neurons and the expression of toll like receptor 4 (TLR4)/myeloid differentiation primary response 88 (Myd88)/nuclear factor (NF)‑κB signal pathway‑associated factors in cardiopulmonary bypass (CPB). Sprague Dawley rats were randomly divided into five groups: Sham operation (Sham); CPB; CPB + α7nAChR agonist PHA568487 (PHA); CPB + α7nAChR inhibitor MLA (MLA); and CPB + PHA568487 + TLR4 antagonist (CPT). Blood and brain tissue samples were harvested at 12 h following the withdrawal of CPB. Levels of serum inflammatory factors [interleukin (IL)‑1β, IL‑6 and tumor necrosis factor (TNF)‑α] and brain injury markers [S‑100β and neuron‑specific enolase (NSE)] were measured using ELISA. In addition, pathological histology and apoptosis changes were observed using hematoxylin and eosin staining, and Tunnel assays. Quantitative polymerase chain reaction and western blot assays were used to determine the expression of TLR4, Myd88 and NF‑κB mRNA, and protein in the hippocampus. The morphology of hippocampal pyramidal cells in the Sham group was observed to be normal. Pyramidal cells in the CPB, MLA and CPT groups were loosely arranged, and the baselines had disappeared, with clear nucleus pyknosis and neuronal apoptosis. Furthermore, the cells in the PHA group were slightly damaged. IL‑1β, IL‑6, TNF‑α, S‑100β and NSE expression levels in the CPB, MLA, and CPT groups were significantly higher compared with that in the Sham group (P<0.05). Compared with CPB group, the expression of inflammatory cytokines in the PHA group was significantly lower (P<0.05). The expression of TLR4, Myd88 and NF‑κB mRNA, and protein in the hippocampus of CPB, MLA and CPT groups were significantly higher compared with that in the Sham group, and the PHA group expression was significantly lower compared with the CPB group (P<0.05). α7nAChRs agonist can inhibit the apoptosis of rat brain neurons induced by CPB, and may protect against brain injury through the TLR4/Myd88/NF‑κB signaling pathway.

Related Articles

Journal Cover

October-2017
Volume 16 Issue 4

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Chen K, Sun Y, Diao Y, Ji L, Song D and Zhang T: α7 nicotinic acetylcholine receptor agonist inhibits the damage of rat hippocampal neurons by TLR4/Myd88/NF‑κB signaling pathway during cardiopulmonary bypass. Mol Med Rep 16: 4770-4776, 2017.
APA
Chen, K., Sun, Y., Diao, Y., Ji, L., Song, D., & Zhang, T. (2017). α7 nicotinic acetylcholine receptor agonist inhibits the damage of rat hippocampal neurons by TLR4/Myd88/NF‑κB signaling pathway during cardiopulmonary bypass. Molecular Medicine Reports, 16, 4770-4776. https://doi.org/10.3892/mmr.2017.7166
MLA
Chen, K., Sun, Y., Diao, Y., Ji, L., Song, D., Zhang, T."α7 nicotinic acetylcholine receptor agonist inhibits the damage of rat hippocampal neurons by TLR4/Myd88/NF‑κB signaling pathway during cardiopulmonary bypass". Molecular Medicine Reports 16.4 (2017): 4770-4776.
Chicago
Chen, K., Sun, Y., Diao, Y., Ji, L., Song, D., Zhang, T."α7 nicotinic acetylcholine receptor agonist inhibits the damage of rat hippocampal neurons by TLR4/Myd88/NF‑κB signaling pathway during cardiopulmonary bypass". Molecular Medicine Reports 16, no. 4 (2017): 4770-4776. https://doi.org/10.3892/mmr.2017.7166