Galangin protects human rheumatoid arthritis fibroblast‑like synoviocytes via suppression of the NF‑κB/NLRP3 pathway

  • Authors:
    • Qiang Fu
    • Yuzhong Gao
    • Hui Zhao
    • Zaijun Wang
    • Jian Wang
  • View Affiliations

  • Published online on: August 22, 2018     https://doi.org/10.3892/mmr.2018.9422
  • Pages: 3619-3624
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Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune disease that significantly affects patient quality of life. Galangin is an extract with multiple health benefits, including anti‑oxidative, anti‑proliferative, immunoprotective and cardioprotective effects. However, to the best of the authors' knowledge, no detailed studies have investigated its regulatory effects on the nuclear factor (NF)‑κB/NLR family pyrin domain containing 3 (NLRP3) signaling pathway. The present study aimed to investigate the protective mechanism of galangin in RA fibroblast‑like synoviocytes with regards to the NF‑κB/NLRP3 signaling pathway. Human RA fibroblast‑like synovium cells (RAFSCs) were treated with lipopolysaccharide (LPS) to induce inflammation. The levels of interleukin (IL)‑1β, tumor necrosis factor (TNF)‑α, IL‑18, inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)‑2, prostaglandin E2 (PGE2), and nitric oxide (NO) were measured by enzyme‑linked immunosorbent assay or western blotting in the absence or presence of different concentrations of galangin. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were additionally evaluated. Furthermore, factors involved in the NF‑κB/NLRP3 pathway, including NLRP3, apoptosis‑associated speck‑like protein containing A, IL‑1β, pro‑caspase‑1, caspase‑1, phosphorylated (p)‑NF‑κB inhibitor α and p‑NF‑κB, were assessed by western blotting. The results revealed that LPS significantly stimulated IL‑1β, TNF‑α, IL‑18, PGE2, NO, iNOS, COX‑2 and NF‑κB/NLRP3 factor expression, compared with the control. SOD activity was reduced. Pre‑treatment with galangin significantly attenuated the effects of LPS, and galangin was demonstrated to have effective anti‑oxidative properties. In conclusion, galangin protected RAFSCs through downregulation of the NF‑κB/NLRP3 signaling pathway. These findings suggested that galangin may provide a novel direction for the development of RA therapies in the future.
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October-2018
Volume 18 Issue 4

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

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Spandidos Publications style
Fu Q, Gao Y, Zhao H, Wang Z and Wang J: Galangin protects human rheumatoid arthritis fibroblast‑like synoviocytes via suppression of the NF‑κB/NLRP3 pathway. Mol Med Rep 18: 3619-3624, 2018
APA
Fu, Q., Gao, Y., Zhao, H., Wang, Z., & Wang, J. (2018). Galangin protects human rheumatoid arthritis fibroblast‑like synoviocytes via suppression of the NF‑κB/NLRP3 pathway. Molecular Medicine Reports, 18, 3619-3624. https://doi.org/10.3892/mmr.2018.9422
MLA
Fu, Q., Gao, Y., Zhao, H., Wang, Z., Wang, J."Galangin protects human rheumatoid arthritis fibroblast‑like synoviocytes via suppression of the NF‑κB/NLRP3 pathway". Molecular Medicine Reports 18.4 (2018): 3619-3624.
Chicago
Fu, Q., Gao, Y., Zhao, H., Wang, Z., Wang, J."Galangin protects human rheumatoid arthritis fibroblast‑like synoviocytes via suppression of the NF‑κB/NLRP3 pathway". Molecular Medicine Reports 18, no. 4 (2018): 3619-3624. https://doi.org/10.3892/mmr.2018.9422