BBR affects macrophage polarization via inhibition of NF-κB pathway to protect against T2DM-associated periodontitis

IF 3.4 3区 医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE
Siying Xia, Rui Jing, Mingyan Shi, Yanan Yang, Meiting Feng, Li Deng, Lijun Luo
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Abstract

Background and Objective

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.

Methods

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.

Results

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.

Conclusions

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.

BBR 通过抑制 NF-κB 通路影响巨噬细胞极化,从而预防 T2DM 相关性牙周炎。
背景和目的:牙周炎与多种全身性疾病的发生密切相关,其中2型糖尿病(T2DM)与牙周炎的发病机制存在双向关系。本研究旨在探讨小檗碱(BBR)在T2DM牙周炎中的作用及相关机制:方法:采用实时定量 PCR(RT-qPCR)技术检测牙周炎症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)小鼠中建立实验性牙周炎模型,模型建立 7 天后给予 BBR。利用微型计算机断层扫描图像测量各组小鼠的牙槽骨损失(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,利用 Western 印迹和 RT-qPCR,探讨了 BBR 影响牙周炎微环境中巨噬细胞极化的信号通路:结果:BBR抑制了牙周炎微环境中的M1极化,刺激了M2极化。在 WT 和 T2DM 牙周炎模型中,BBR 降低了 ABL。在 WT 和 T2DM 模型小鼠的牙龈中,BBR 可减少促炎细胞因子的产生,增加抗炎细胞因子的表达。最终,BBR 通过抑制 NF-κB 通路对牙周炎产生抗炎作用:结论:BBR通过抑制NF-κB途径影响巨噬细胞极化,对T2DM相关性牙周炎具有治疗作用,这可能对T2DM相关性牙周炎的新药物治疗具有启示意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of periodontal research
Journal of periodontal research 医学-牙科与口腔外科
CiteScore
6.90
自引率
5.70%
发文量
103
审稿时长
6-12 weeks
期刊介绍: The Journal of Periodontal Research is an international research periodical the purpose of which is to publish original clinical and basic investigations and review articles concerned with every aspect of periodontology and related sciences. Brief communications (1-3 journal pages) are also accepted and a special effort is made to ensure their rapid publication. Reports of scientific meetings in periodontology and related fields are also published. One volume of six issues is published annually.
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