Diosmetin alleviates periodontitis by inhibiting oxidative stress and pyroptosis through Nrf2/NF κB/NLRP3 axis

Abstract

Purpose: To investigate the therapeutic role of diosmetin in periodontitis and its probable mechanism of action.Methods: Lipopolysaccharide (LPS) was used to induce periodontitis in periodontal cells. Cell viability and apoptosis in response to LPS and diosmetin were evaluated using MTT and TUNEL assays. The oxidative stress and inflammatory responses in LPS-induced periodontitis and diosmetin effects in periodontal cells were detected using enzyme-linked immunosorbent assay (ELISA). In addition, the roles of diosmetin in pyroptosis and Nrf2/NF-kappa B/NLRP3 pathway were analyzed by immunoblot assays.Results: Diosmetin increased the viability of LPS-induced periodontal cells (p < 0.01). Diosmetin also alleviated the oxidative stress of periodontal cells (p < 0.01), reduced the secretion of pro-inflammatory factors in periodontal cells, and inhibited cell pyroptosis (p < 0.01). Diosmetin also mediated Nrf2/NFkappa B/NLRP3 pathway (p < 0.01).Conclusion: Diosmetin alleviates periodontitis by inhibiting oxidative stress and pyroptosis through Nrf2/NF-κB/NLRP3 axis. However, in vivo studies are required to validate this finding.