Anti-inflammatory activity of fisetin in human gingival fibroblasts treated with lipopolysaccharide

Abstract

Fisetin is an anti-inflammatory flavonoid; however, its anti-inflammatory mechanism is not yet understood. In this study, we evaluated the anti-inflammatory effect of fisetin and its association with mitogen-activated protein kinase (MAPK) and nuclear factor kappa-beta pathways in human gingival fibroblasts (HGFs) treated with lipopolysaccharide (LPS) obtained from Porphyromonas gingivalis. The cell signaling, cell viability, and cyclooxygenase-2 (COX-2) expression of HGFs treated with various concentrations (0, 1, 5, 10, and 15 μM) of fisetin were measured by cell viability assay (MTT), Western blotting, and reverse transcriptase polymerase chain reaction analysis on COX-2. We found that fisetin significantly reduced the synthesis and expression of prostaglandin E2 in HGFs treated with LPS. Activation of extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38 MAPK was suppressed consistently by fisetin in HGFs treated with LPS. The data indicate that fisetin inhibits MAPK activation and COX-2 expression without affecting cell viability. These findings may be valuable for understanding the mechanism of the effect of fisetin on periodontal disease.

Keywords::

• human gingival fibroblasts
• lipopolysaccharide
• flavonoids
• mitogen activated protein kinases
• cyclooxygenase-2
• fisetin

Acknowledgments

The work was financially supported by grant from Dirección General de Personal Académico [DGAPA] PAPITT IN209412-3. The authors equally acknowledge the assistance of Carmen Muñoz-Seca in the revision of the text.

Declaration of interest

The authors declare that there is no conflict of interest.