Non-Clinical Evaluation Center Biomedical Research Institute, Jeonbuk National University Hospital, Jeonju, Jeonbuk, 54907, South Korea.
Research Institute of Clinical Medicine of Jeonbuk National University-Biomedical Research Institute of Jeonbuk National University Hospital, Jeonju, Jeonbuk, 54907, Republic of Korea.
Sci Rep. 2023 Aug 8;13(1):12861. doi: 10.1038/s41598-023-39853-5.
Periodontitis is an infectious inflammation in the gums characterized by loss of periodontal ligaments and alveolar bone. Its persistent inflammation could result in tooth loss and other health issues. Ixeris dentata (IXD) and Lactobacillus gasseri media (LGM) demonstrated strong antioxidant activity, which may prevent oxidative and inflammatory periodontitis. Here, IXD and LGM extracts were investigated for antioxidative activity against oral discomfort and evaluated for their synergistic effect against oxidative and inflammatory periodontitis in a mouse model. IXD/LGM suppressed pro-inflammatory cytokines like interleukin (IL)-1β, IL-6, and TNF-α. Additionally, it reduced pro-inflammatory mediators, nitric oxide, iNOS (inducible nitric oxide synthase), and COX-2 (cyclooxygenase-2) and enhanced AKT, Nrf2, and HO-1 activation. Similarly, IXD/LGM treatment elevated osteogenic proteins and mRNAs; alkaline phosphatase, collagen type 1 (COL1), osteopontin (OPN), and runt-related transcription factor 2 (RUNX2). Hematoxylin and Eosin (H&E) staining and micro-CT analysis confirm the positive impact of IXD/LGM on the periodontal structure and its associated inflammation. These findings demonstrate that IXD/LGM inhibits oxidative stress, periodontal inflammation, and its resultant alveolar bone loss in which Akt (also known as protein kinase B)-nuclear factor-erythroid 2-related factor 2 (Nrf2)-hemoxygenase-1 (HO-1) signaling is involved. Thus, IXD/LGM is a potential candidate against oxidative/inflammatory stress-associated periodontitis.
牙周炎是一种牙龈感染性炎症，其特征是牙周韧带和牙槽骨丧失。其持续的炎症可能导致牙齿脱落和其他健康问题。苦碟子和发酵乳杆菌培养基显示出很强的抗氧化活性，这可能预防氧化和炎症性牙周炎。在这里，研究了苦碟子和发酵乳杆菌培养基提取物的抗氧化活性，以对抗口腔不适，并在小鼠模型中评估其对氧化和炎症性牙周炎的协同作用。苦碟子/发酵乳杆菌培养基抑制促炎细胞因子，如白细胞介素（IL）-1β、IL-6 和 TNF-α。此外，它还降低了促炎介质一氧化氮、诱导型一氧化氮合酶（iNOS）和环氧化酶-2（COX-2），并增强了 AKT、Nrf2 和 HO-1 的激活。同样，苦碟子/发酵乳杆菌培养基治疗提高了成骨蛋白和 mRNA 的水平；碱性磷酸酶、胶原类型 1（COL1）、骨桥蛋白（OPN）和 runt 相关转录因子 2（RUNX2）。苏木精-伊红（H&E）染色和微 CT 分析证实了苦碟子/发酵乳杆菌培养基对牙周结构及其相关炎症的积极影响。这些发现表明，苦碟子/发酵乳杆菌培养基抑制氧化应激、牙周炎及其导致的牙槽骨丢失，其中 Akt（也称为蛋白激酶 B）-核因子-红细胞 2 相关因子 2（Nrf2）-血红素加氧酶-1（HO-1）信号通路参与其中。因此，苦碟子/发酵乳杆菌培养基是一种针对氧化/炎症应激相关牙周炎的潜在候选药物。
