Quercetin protects oral mucosal keratinocytes against lipopolysaccharide-induced inflammatory toxicity by suppressing the AKT/AMPK/mTOR pathway

Background Cytokines can induce a chronic inflammatory response in the periodontium, leading to periodontitis. Quercetin, a naturally occuring flavonoid, has been shown to inhibit periodontitis, but how it works is poorly understood. In this study, we assessed the impact of quercetin on lipopolysaccharide (LPS)-induced inflammatory damage in oral mucosal keratinocytes (hOMK107) and explored its underlying mechanism.Methods The viability and apoptosis of hOMK107 cells were measured after exposure to LPS, followed or not by quercetin. The production of IL-1β, IL-6, IL-8, TNF-ɑ, iNOS, and COX-2 was quantified by enzyme-linked immunosorbent assay (ELISA), while levels of Akt, AMPK, and mTOR and their phosphorylation were detected semi-quantitatively by western blotting.Results Quercetin significantly improved cell viability and apoptosis by reversing LPS-induced upregulation of Bax and downregulation of Bcl-2 in hOMK107 cells. Quercetin decreased the production of IL-1β, IL-6, IL-8, TNF-ɑ, iNOS, and COX-2, as well as signal transduction via the Akt/AMPK/mTOR pathway. Inhibitors of Akt, AMPK, and mTOR strengthened the anti-apoptotic effects of quercetin, while agonists of Akt, AMPK, or mTOR or Akt overexpression weakened the anti-apoptotic effects.Conclusion These results indicate that quercetin may have a potential protective effect against the chronic inflammation-related periodontitis via suppressing Akt/AMPK/mTOR pathway.