Tectochrysin Alleviates Periodontitis by Modulating M2/M1 Macrophage Ratio and Oxidative Stress Via Nuclear Factor Kappa B/Heme Oxygenase-1/Nuclear Factor Erythroid 2-Related Factor 2 Pathway

BackgroundTectochrysin suppresses several diseases. In this study, we aimed to explore the effects of tectochrysin ona rat model of periodontitis PDS).MethodsMale Sprague-Dawley (SD) rats were subjected to ligature to induce periodontitis. Bone parameters were analyzed using micro-computed tomography and periodontal tissues were evaluated using Masson's, hematoxylin and eosin, and tartrate-resistant acid phosphatase staining. The expression of HO-1, Nrf2, CD206, Arg-1, and iNOS was evaluated using immunohistochemistry. Malondialdehyde (MDA), reduced glutathione (GSH), and superoxide dismutase (SOD) levels and IL-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha,and NF-kappa B and Nrf2/HO-1 were analyzed.ResultsTectochrysin reduced alveolar bone loss, promoted new bone formation, and inhibited osteoclast formation in periodontitis rats. It decreased the number of inflammatory cells and the levels of IL-1 beta, IL-6, and TNF-alpha, indicating a reduction in inflammation. Tectochrysin restored the Arg-1/iNOS ratio, indicating M2 macrophage polarization, and inhibited the NF-kB pathway. Tectochrysin restored GSH and SOD levels, inhibited MDA content, and activated the HO-1/Nrf2 pathway.ConclusionTectochrysin alleviates PDS in rats by modulating the M2/M1 macrophage ratio via the NF-kB pathway and suppressing oxidative stress via the HO-1/Nrf2 pathway.