口腔医学研究

口腔医学研究 ›› 2025, Vol. 41 ›› Issue (6): 521-528.DOI: 10.13701/j.cnki.kqyxyj.2025.06.012

• 牙周病学研究 • 上一篇    下一篇

卵泡激素相互作用蛋白1对牙周炎症的调控研究

张彩霞1, 周怡文2#, 闻娟1, 黄子维1, 林爽1, 杨任1, 李煌1*, 李贵凤1*   

  1. 1.南京大学医学院附属口腔医院正畸科,南京市口腔医院,南京大学口腔医学研究所 江苏 南京 210000;
    2.常州市第一人民医院,苏州大学第三附属医院口腔科 江苏 常州 213000
  • 收稿日期:2024-11-05 出版日期:2025-06-28 发布日期:2025-06-25
  • 通讯作者: *李煌,E-mail:Lihuang76@nju.edu.cn李贵凤,E-mail:407638612@qq.com
  • 作者简介:张彩霞(1990~ ),女,湖北襄阳人,硕士,主治医师,主要研究牙周炎和颞下颌关节骨关节炎的发病机制和治疗。周怡文(1998~ ),女,江苏常州人,博士,医师,研究方向:骨性错牙合畸形发病机制及治疗。#为共同第一作者
  • 基金资助:
    南京大学医学院附属口腔医院2015学科带头人后备人才资助项目(编号:0223A101)南京市卫生科技发展一般项目(编号:YKK22178)江苏省基础研究计划(自然科学基金)面上项目(编号:SBK2021021787)江苏省卫健委重点项目(编号:ZD2022025)

Regulation of Folliculin Interacting Protein 1 on Periodontitis

ZHANG Caixia1, ZHOU Yiwen2#, WEN Juan1, HUANG Ziwei1, LIN Shuang1, YANG Ren1, LI Huang1*, LI Guifeng1*   

  1. 1. Department of Orthodontics, Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing 210000, China;
    2. Department of Stomatology, the First People's Hospital of Changzhou, the Third Affiliated Hospital of Soochow University, Changzhou 213000, China
  • Received:2024-11-05 Online:2025-06-28 Published:2025-06-25

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摘要： 目的: 探索卵泡激素相互作用蛋白1(folliculin interacting protein 1,FNIP1)对牙周炎症反应的调控作用及其机制。方法: 收集牙周健康患者和牙周炎患者的牙龈组织,免疫荧光染色检测FNIP1表达变化。体外培养人牙周膜干细胞,分为对照组、牙龈卟啉单胞菌 (Porphyromonas gingivalis, P.g)组、FNIP1敲减组、FNIP1敲减+P.g组、FNIP1敲减+P.g+腺苷酸活化蛋白激酶(adenosine 5‘-monophosphate-activated protein kinase, AMPK)抑制剂组。Western blot检测FNIP1、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、AMPK、p-AMPK、过氧化物酶体增殖受体γ辅激活因子1α(peroxisome proliferators-activated receptor γ coactivator lalpha, PGC-1α)及线粒体复合物相关因子蛋白表达;流式细胞仪及激光共聚焦显微镜检测细胞活性氧含量及线粒体膜电位变化。结果: 与健康牙龈相比,牙周炎患者牙龈组织FNIP1表达明显升高。P.g刺激能提高人牙周膜干细胞FNIP1、TNF-α表达,降低细胞 p-AMPK、PGC-1α表达,导致线粒体功能紊乱;FNIP1 敲减后可以缓解该现象。而AMPK抑制剂可以部分抵消FNIP1敲减对牙周炎症及线粒体功能紊乱的缓解作用。结论: FNIP1可以通过AMPK通路调控牙周炎症及牙周膜干细胞线粒体功能紊乱,抑制FNIP1可能可以缓解牙周炎的发生发展。

关键词: 卵泡激素相互作用蛋白1, 腺苷酸活化蛋白激酶, 牙周炎, 牙龈卟啉单胞菌, 牙周膜干细胞

Abstract: Objective: To explore the role and mechanism of folliculin interacting protein 1 (FNIP1) in periodontitis. Methods: Gingival tissues were collected from healthy volunteers and periodontitis patients. FNIP1 expression in the gingival tissues was detected by immunohistochemistry. Human periodontal stem cells (PDLSCs) were divided into control group (Con), Porphyromonas gingivalis group (P.g), FNIP1 siRNA group, P.g+FNIP1 siRNA group, and P.g+FNIP1 siRNA+Compound C (AMPK inhibitor) group. Western blot was used to detect the expression of FNIP1, tumor necrosis factor-α (TNF-α), adenosine 5‘-monophosphate-activated protein kinase (AMPK), p-AMPK, peroxisome proliferators-activated receptor γ coactivator 1 lalpha (PGC-1α), and factors associated with mitochondrial. Flow cytometry and confocal microscopy were used to detect the reactive oxygen species (ROS) content and mitochondrial membrane potential changes. Results: Compared with healthy gingiva, FNIP1 expression was significantly increased in periodontitis’s gingival tissues. P.g could increase the expression of FNIP1 and TNF-α in PDLSCs, decrease the expression of p-AMPK and PGC-1α, leading to mitochondrial dysfunction. FNIP1 siRNA could alleviate these phenomenons (P<0.05). However, Compound C could counteract the alleviation of FNIP1 siRNA partially. Conclusion: FNIP1 can regulate the inflammation and mitochondrial dysfunction of periodontal ligament stem cells through the AMPK pathway. Inhibiting FNIP1 may be able to alleviate the development of periodontitis.

Key words: folliculin interacting protein 1, adenosine 5‘-monophosphate-activated protein kinase, periodontitis, Porphyromonas gingivalis, periodontal ligament stem cells