TPCA ‐1 negatively regulates inflammation mediated by NF‐κB pathway in mouse chronic periodontitis model

AbstractThe dysregulation of immune system plays a crucial function in periodontitis development. Pro ‐inflammatory cytokines are thought to be critical for the generation and development of periodontitis. The enhanced activity of osteoclasts contributes to periodontitis pathogenesis. Nuclear factor‐κB (NF‐κB) signaling pathway directly enhances osteoclast differentiation and maturation. 2‐ [(aminocarbonyl)amino]‐5‐(4‐fluorophenyl)‐3‐thiophenecarboxamide (TPCA‐1) is a IκB kinases (IKK) inhibitor. This research aimed to investigate whether TPCA‐1 had influence on the pathogenesis of chronic periodontitis. Mouse chronic periodontitis was induced by anin vivo ligature ‐induced periodontitis model. TPCA‐1 was intravenous injected into mice after chronic periodontitis induction. Bone marrow‐derived macrophages were cultured in macrophage colony‐stimulating factor (M‐CSF)‐conditioned media with receptor activator of nuclear factor‐kappa B ligand (RANKL ) inducein vitro osteoclast differentiation. Western blot was used to analyze protein levels and mRNA levels were analyzed through qRT ‐PCR. TPCA‐1 promoted osteoclastogenesis and osteoclast‐related gene expressionin vitro. The production of pro ‐inflammatory cytokines in osteoclasts induced by lipopolysaccharides was inhibited by TPCA‐1in vitro.In vitro TPCA ‐1 treatment inhibitedAggregatibacter actinomycetemcomitans (A.a) ‐induced expression of pro‐inflammatory cytokines and NF...

Source: Molecular Oral Microbiology - March 30, 2021 Category: Microbiology Authors: Bo Wang, Shizhu Bai, Jiang Wang, Nan Ren, Rui Xie, Geng Cheng, Yan Yu Tags: ORIGINAL ARTICLE Source Type: research