牙周疾病是一种慢性炎症性疾病，导致牙齿的支持结构，包括牙龈、牙周韧带、牙槽骨和根胶质逐渐破坏。最近，使用天然化合物缓解牙周炎（PD）症状的兴趣正日益增加。Avenanthramide-C（Avn-C）是仅存在于燕麦中的多酚。它被认为具有各种生物特性。迄今为止，尚未证实Avn-C对PD发病机制的影响。因此，本研究旨在验证Avn-C对体外和体内牙周炎病理过程中牙周炎炎症和随后的牙槽骨侵蚀的保护作用。用脂多糖和促炎细胞因子—IL-1β和肿瘤坏死因子α（TNF-α）诱导的分泌基质金属蛋白酶1（MMP1）、MMP3、白细胞介素（IL）-6、IL-8和COX2等分解因子的表达，通过Avn-C处理对人类牙龈成纤维细胞和牙周韧带细胞产生显著抑制作用。此外，通过牙索诱导的PD小鼠模型内龈注射Avn-C可以改善牙槽骨侵蚀。分子机制研究揭示了Avn-C对降解因子上调的抑制作用是通过被IL-1β激活的ERK（细胞外信号调控激酶）和NF-κB途径以及被TNF-α激活的p38 MAPK和JNK信号途径介导的。基于本研究，我们推荐Avn-C可能是一种可以应用于PD治疗的新型天然化合物。

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.