Quercetin Decreases Th17 Production by Down-Regulation of MAPK- TLR4 Signaling Pathway on T Cells in Dental Pulpitis

Statement of the problem: quercetin is a pharmacological flavonoid that can inhibit high mobility group box1 (hmgb1) protein, a non-histone nuclear protein that is implicated in inflammation. th17 cells are important cells in the pathogene-sis of inflammation. pulpitis is the inflammation of dental pulp, which usually is accompanied by pain. quercetin may alleviate this inflammation. purpose: the current study aimed to compare blocking of hmgb1 function and stimulation of hmgb1 function with quercetin and investigate the effects of the blockage on t helper 17 (th17) cells and mitogen-activated protein kinase toll-like receptor 4 (mapk-tlr4) signaling pathway. materials and method: t cells isolated from the pulp involved with pulpitis and the normal pulp were cultured. the cells suspensions were plated in 6-wells culture plates and stimulated with 0.5 μg/ml of hmgb1 for 2, 4, 8, and 12 hours. for blocking tlr4, 10 μg/ml rabbit anti-human tlr4 antibody was added 1 hour before treatment with hmgb1. results: the level of these cytokines decreased; moreover, western blot data showed that quercetin could decrease mapk signaling pathway by means of inhi-bition of hmgb1 on t cells. the results showed the reduction of tlr4 pathway and th17 cell polarization. conclusion: our results indicated that the levels of il-17, il-33, and il-6 in su- pernatants from patients’ cultured t cells were increased after stimulation with hmgb-1 following employing quercetin. it also could inhibit mapk signaling pathway, which subsequently could decrease th17 production and il-17. quercetin could decrease pro-inflammatory cytokines and il-17 production.