Open Access

PYNOD reduces microglial inflammation and consequent neurotoxicity upon lipopolysaccharides stimulation

  • Authors:
    • Qi Zeng
    • Chaofeng Hu
    • Renbin Qi
    • Daxiang Lu
  • View Affiliations

  • Published online on: April 30, 2018     https://doi.org/10.3892/etm.2018.6108
  • Pages: 5337-5343
  • Copyright: © Zeng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

PYNOD, a nod‑like receptors (NLR)‑like protein, was indicated to inhibit NF‑κB activation, caspase‑1‑mediated interleukin (IL)‑1β release and cell apoptosis in a dose‑dependent manner. Exogenous addition of recombinant PYNOD to mixed glial cultures may suppress caspase‑1 activation and IL‑1β secretion induced by Aβ. However, to the best of our knowledge, there no study has focused on the immunoregulatory effects of PYNOD specifically in microglia. The present study aimed to explore the roles of PYNOD involved in the lipopolysaccharides (LPS)‑induced microglial inflammation and consequent neurotoxicity. Murine microglial BV‑2 cells were transfected with pEGFP‑C2‑PYNOD (0-5.0 µg/ml) for 24 h and incubated with or without LPS (1 µg/ml) for a further 24 h. Cell viability was determined using MTT assay and the secretion of nitric oxide (NO), IL‑1β and caspase‑1 was measured using the Griess method or ELISA. Protein expression levels of NF‑κB p65 and inducible nitric oxide synthase (iNOS) were detected by immunofluorescent staining and/or western blot analysis. Co‑culture of BV‑2 cells with human neuroblastoma cell line SK‑N‑SH was performed in Transwell plates and the cell viability and apoptosis (using flow cytometry) of SK‑N‑SH cells were determined. Results indicated that PYNOD overexpression inhibited NO secretion and iNOS protein expression induced by LPS in BV‑2 cells, with no detectable cytotoxicity. PYNOD overexpression also reduced the secretion of IL‑1β and caspase‑1 from BV‑2 cells upon LPS stimulation. These effects were dose‑dependent. Additionally, PYNOD overexpression prevented LPS‑induced nuclear translocation of NF‑κB p65 in BV‑2 cells. The growth‑inhibitory and apoptosis‑promoting effects of BV‑2 cells towards SK‑N‑SH cells were alleviated as a result of PYNOD overexpression. In conclusion, PYNOD may mitigate microglial inflammation and consequent neurotoxicity.
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June-2018
Volume 15 Issue 6

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Zeng Q, Hu C, Qi R and Lu D: PYNOD reduces microglial inflammation and consequent neurotoxicity upon lipopolysaccharides stimulation. Exp Ther Med 15: 5337-5343, 2018
APA
Zeng, Q., Hu, C., Qi, R., & Lu, D. (2018). PYNOD reduces microglial inflammation and consequent neurotoxicity upon lipopolysaccharides stimulation. Experimental and Therapeutic Medicine, 15, 5337-5343. https://doi.org/10.3892/etm.2018.6108
MLA
Zeng, Q., Hu, C., Qi, R., Lu, D."PYNOD reduces microglial inflammation and consequent neurotoxicity upon lipopolysaccharides stimulation". Experimental and Therapeutic Medicine 15.6 (2018): 5337-5343.
Chicago
Zeng, Q., Hu, C., Qi, R., Lu, D."PYNOD reduces microglial inflammation and consequent neurotoxicity upon lipopolysaccharides stimulation". Experimental and Therapeutic Medicine 15, no. 6 (2018): 5337-5343. https://doi.org/10.3892/etm.2018.6108