Myricetin Inhibition of Peptidoglycan-Induced COX-2 Expression in H9c2 Cardiomyocytes

Peptidoglycan (PGN) is a cell wall constituent in dental plaque bacteria that triggers inflammatory responses. PGN binds Toll-like receptors, leading to increases in prostaglandin E2 and interleukin-1β, which play crucial roles in the inflammatory response and tissue destruction. Dental surgery can give plaque bacteria access to blood circulation, thereby creating a risk of septic inflammation of the endocardium. Plant-derived flavonoids have been reported to reduce inflammatory cytokine secretion by host cells. In the present study, we investigated the effects of flavonoid myricetin on expression of cyclooxygenase 2 (COX-2) in the H9c2 cells treated with PGN from Streptococcus sanguinis, a bacterial constituent of dental plaque associated with infective endocarditis. Myricetin exposure resulted in dose-dependent suppression of PGN-induced COX-2 expression, diminished phosphorylation of p38, extracellular signal regulated kinase 1/2, and c-Jun N-terminal kinase, and reduced IκB-α degradation, consistent with decreased COX-2 activity. In conclusion, the aforementioned results suggest that myricetin is useful for moderating the inflammatory response in infective endocarditis.