Metformin ameliorates HMGB1-mediated oxidative stress through mTOR pathway in experimental periodontitis

• DOI: 10.1016/j.gendis.2021.06.003
• Publication Date: 2021-06-30T16:16:41Z
• Authors: Boyang Sun; Siqi Ying; Qian Ma; Han Li; Jie Li; Jinlin Song
• Keywords: Viability assay; HMGB1

Periodontitis is an oral chronic inflammatory disease. Inhibiting tissue destruction and promoting regeneration are important means for the treatment of periodontitis. Metformin not only has hypoglycemic effect but also anti-inflammatory effect. been shown to inhibit oxidative stress activate autophagy through AMPK/mTOR pathway. High mobility group box 1 (HMGB1) implicated in pathogenesis many diseases including periodontitis, it can participate induction stress. HMGB1 regulator under stress, which mTOR However, clear whether metformin related its mechanism process Cell viability expression cytokines were clarified by Counting Kit-8, real-time PCR enzyme-linked immunosorbent assay. Western blot immunofluorescence conducted determine intracellular localization autophagy-associated proteins vitro. Experimental periodontitis mice model was induced administering a ligature. Immunohistochemistry performed detect vivo. The results CCK-8, PCR, assay, showed lipopolysaccharide (LPS) inhibited cell viability, increased at dose-independent manner. reduce LPS. It improves pathway LPS down-regulates expression. In addition, attenuated alveolar bone resorption ligation. This study provides new evidence that potential drug may be target periodontal intervention.