Myricetin suppresses lipoteichoic acid-induced interleukin-1beta and cyclooxygenase-2 expression in human gingival fibroblasts

摘要

Periodontitis is an inflammatory disease affecting the connective tissue and supporting bone surrounding the teeth. In periodontitis, human gingival fibroblasts (HGFs) synthesize IL-1beta, causing a progressive inflammatory response. Flavones demonstrate a variety of biological activity: among others, they possess anti-inflammatory properties. Myricetin is a flavone with a strong antiinflammatory activity. The objective of this study was to evaluate the effect of the flavonoid myricetin on HGFs underinflammatory conditions induced by lipoteichoic acid (LTA). the effect of myricetin on HGFs was assessed by measuring cell viability, signaling pathways and IL-1beta expression and synthesis. It was found that, over time, myricetin did not affect cell viability. However, it inhibited activation of p38 and extracellular-signal-regulated kinase-1/2 in LTA-treated HGFs and also blocked IkappaB degradation and cyclooxygenase-2 and prostaglandin E2 synthesis and expression. These findings suggest that myricetin has therapeutic effects in the form of controlling LTA-induced inflammatory responses.