Avenanthramide-C Shows Potential to Alleviate Gingival Inflammation and Alveolar Bone Loss in Experimental Periodontitis

Mol Cells. 2023 Oct 31;46(10):627-636. doi: 10.14348/molcells.2023.0109. Epub 2023 Aug 29.

Abstract

Periodontal disease is a chronic inflammatory disease that leads to the gradual destruction of the supporting structures of the teeth including gums, periodontal ligaments, alveolar bone, and root cementum. Recently, interests in alleviating symptoms of periodontitis (PD) using natural compounds is increasing. Avenanthramide-C (Avn-C) is a polyphenol found only in oats. It is known to exhibit various biological properties. To date, the effect of Avn-C on PD pathogenesis has not been confirmed. Therefore, this study aimed to verify the protective effects of Avn-C on periodontal inflammation and subsequent alveolar bone erosion in vitro and in vivo. Upregulated expression of catabolic factors, such as matrix metalloproteinase 1 (MMP1), MMP3, interleukin (IL)-6, IL-8, and COX2 induced by lipopolysaccharide and proinflammatory cytokines, IL-1β, and tumor necrosis factor α (TNF-α), was dramatically decreased by Avn-C treatment in human gingival fibroblasts and periodontal ligament cells. Moreover, alveolar bone erosion in the ligature-induced PD mouse model was ameliorated by intra-gingival injection of Avn-C. Molecular mechanism studies revealed that the inhibitory effects of Avn-C on the upregulation of catabolic factors were mediated via ERK (extracellular signal-regulated kinase) and NF-κB pathway that was activated by IL-1β or p38 MAPK and JNK signaling that was activated by TNF-α, respectively. Based on this study, we recommend that Avn-C may be a new natural compound that can be applied to PD treatment.

Keywords: alveolar bone loss; avenanthramide-C; gingival fibroblasts; inflammation; periodontitis.

MeSH terms

  • Alveolar Bone Loss* / drug therapy
  • Alveolar Bone Loss* / metabolism
  • Animals
  • Humans
  • Inflammation / drug therapy
  • Interleukin-6 / metabolism
  • Mice
  • Periodontitis* / drug therapy
  • Periodontitis* / metabolism
  • Periodontitis* / pathology
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Tumor Necrosis Factor-alpha
  • avenanthramide-2C
  • Interleukin-6

Grants and funding

ACKNOWLEDGMENTS This work was supported by the National Research Foundation of Korea (NRF) grant, funded by the Korean government (MSIT) (NRF-2019R1A5A2027521, 2021R1A2C3005727, 2022R1C1C2013357), and Chonnam National University Hospital Biomedical Research Institute (BCRI21026). This research was supported by the Korean Fund for Regenerative Medicine (KFRM) grant, funded by the Korean government (the Ministry of Science and ICT, the Ministry of Health & Welfare) (22A0104L1).