BET protein inhibitor apabetalone represses Porphyromonas gingivalis LPS-induced macrophage M1 polarization via regulating miR-130a/STAT3 axis

Periodontitis is a frequent chronic inflammatory disorder destroying periodontium. Recent studies have revealed the role of bromodomain and extraterminal domain inhibitor (BETi) microRNA (miR)-130a in regulating macrophage polarization pro-inflammatory response. However, little known about whether apabetalone (a novel BETi) miR-130a are correlated with state periodontitis by polarization. Here murine RAW264.7 macrophages were applied as an vitro model. After treatment Porphyromonas gingivalis-derived lipopolysaccharide (Pg LPS) apabetalone, expression M1 markers cytokines was assessed using real-time PCR, western blot, enzyme-linked immuno sorbent assay (ELISA). MiR-130a level target gene identified dual luciferase reporter assay. We demonstrated that repressed Pg LPS-induced dose-dependent manner, evidenced decreased inducible nitric oxide synthase (iNOS), CD86, cytokines, increased Arg-1 CD206. Mechanistically, LPS macrophages, whereas effect. Functionally, forced promoted polarization, signal transducer activator transcription (STAT)-3 direct process. Taken together, decreases via miR-130a-3p/STAT3 axis, may be promising for clinical management periodontitis.