Department of Periodontology, Stomatological Hospital and Dental School of Tongji University, Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Shanghai, China.
J Periodontal Res. 2024 Aug;59(4):728-737. doi: 10.1111/jre.13246. Epub 2024 Mar 19.
Periodontitis is intimately associated with the development of various systemic diseases, among which type 2 diabetes mellitus (T2DM) has a bidirectional relationship with the pathogenesis of periodontitis. The objective of the present work was to investigate the role of berberine (BBR) in periodontitis with T2DM and related mechanisms.
The mRNA expression of macrophage polarization-related factors in the microenvironment of periodontal inflammation was detected using real-time quantitative PCR (RT-qPCR). The experimental periodontitis model was constructed in wild-type (WT) and T2DM (db/db) mice, which were administered BBR after 7 days of modeling. Alveolar bone loss (ABL) in each group of mice was measured utilizing micro-computed tomography images. RT-qPCR was performed to analyze the levels of macrophage polarization-related factors in mouse gingiva. Lastly, using western blotting and RT-qPCR, the signaling pathway of BBR affecting macrophage polarization in the microenvironment of periodontitis was explored.
BBR inhibited M1 polarization and stimulated M2 polarization in the periodontitis microenvironment. BBR decreased ABL in the WT and T2DM periodontitis models. And BBR reduced the production of proinflammatory cytokines and increased anti-inflammatory cytokine expression in the gingiva of WT and T2DM model mice. Ultimately, BBR mediates its anti-inflammatory effects on periodontitis through inhibition of the NF-κB pathway.
BBR had a therapeutic effect on T2DM-associated periodontitis via inhibiting the NF-κB pathway to affect macrophage polarization, which may have implications for the new pharmacological treatment of T2DM-associated periodontitis.
牙周炎与多种系统性疾病的发生发展密切相关，其中 2 型糖尿病（T2DM）与牙周炎的发病机制呈双向关系。本研究旨在探讨小檗碱（BBR）在伴 T2DM 牙周炎中的作用及其相关机制。
采用实时定量 PCR（RT-qPCR）检测牙周炎微环境中巨噬细胞极化相关因子的 mRNA 表达。在野生型（WT）和 T2DM（db/db）小鼠中构建实验性牙周炎模型，建模 7 天后给予 BBR。利用微计算机断层扫描图像测量各组小鼠牙槽骨丧失（ABL）。采用 RT-qPCR 分析小鼠牙龈中巨噬细胞极化相关因子的水平。最后，通过 Western blot 和 RT-qPCR 探讨 BBR 影响牙周炎微环境中巨噬细胞极化的信号通路。
BBR 抑制了牙周炎微环境中的 M1 极化并刺激了 M2 极化。BBR 减少了 WT 和 T2DM 牙周炎模型中的 ABL。并且 BBR 降低了 WT 和 T2DM 模型小鼠牙龈中促炎细胞因子的产生，增加了抗炎细胞因子的表达。最终，BBR 通过抑制 NF-κB 通路介导其对牙周炎的抗炎作用。
BBR 通过抑制 NF-κB 通路影响巨噬细胞极化，对 T2DM 相关牙周炎具有治疗作用，这可能为 T2DM 相关牙周炎的新药物治疗提供思路。
