Plantamajoside attenuates inflammatory response in LPS-stimulated human gingival fibroblasts by inhibiting PI3K/AKT signaling pathway

Microb Pathog. 2019 Feb:127:208-211. doi: 10.1016/j.micpath.2018.11.034. Epub 2018 Nov 23.

Abstract

Periodontitis is an important inflammatory disease that often causes by periodontopathic bacteria. The present study, we tested the anti-inflammatory effects of plantamajoside on LPS-stimulated human gingival fibroblasts. Human gingival fibroblasts (HGFs) were stimulated with LPS from Porphyromonas gingivalis. Plantamajoside was administrated 1 h before LPS treatment. The results demonstrated that plantamajoside decreased the production of PGE2, NO, IL-6, and IL-8 in LPS-stimulated HGFs. LPS-induced NF-κB p65 and IκB phosphorylation were also suppressed by plantamajoside. Furthermore, plantamajoside inhibited LPS-induced PI3K and AKT phosphorylation. In conclusion, these results suggested that the mechanism of plantamajoside was through inhibiting PI3K/AKT signaling pathway, which lead to the inhibition of NF-κB activation and inflammatory response.

Keywords: Human gingival fibroblasts; IL-8; LPS; PI3K; Plantamajoside.

MeSH terms

  • Anti-Inflammatory Agents / pharmacology*
  • Catechols / pharmacology*
  • Cells, Cultured
  • Fibroblasts / drug effects*
  • Glucosides / pharmacology*
  • Humans
  • Inflammation Mediators / antagonists & inhibitors
  • Lipopolysaccharides / isolation & purification
  • Lipopolysaccharides / toxicity*
  • Phosphatidylinositol 3-Kinase / metabolism*
  • Porphyromonas gingivalis / chemistry
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Signal Transduction / drug effects*

Substances

  • Anti-Inflammatory Agents
  • Catechols
  • Glucosides
  • Inflammation Mediators
  • Lipopolysaccharides
  • plantamajoside
  • Phosphatidylinositol 3-Kinase
  • Proto-Oncogene Proteins c-akt