口腔医学 ›› 2026, Vol. 46 ›› Issue (3): 174-180.doi: 10.13591/j.cnki.kqyx.2026.03.003

• 基础与临床研究 • 上一篇    下一篇

circRNA_3498抑制自噬促进2型糖尿病小鼠牙周炎症的机制研究

梅幼敏1,2, 黄玲燕2, 沈想3, 王鑫蕾4, 王晓茜1,5()   

  1. 1 口腔疾病研究与防治国家级重点实验室培育建设点, 江苏南京 (210029)
    2 南通市口腔医院(南通大学附属南通口腔医院)牙周病科, 江苏南通 (226001)
    3 南通大学附属医院口腔医疗中心, 江苏南通 (226001)
    4 南通大学附属医院内分泌科, 江苏南通 (226001)
    5 南京医科大学附属口腔医院牙周病科, 江苏省口腔转化医学工程研究中心, 江苏南京 (210029)
  • 收稿日期:2024-10-29 出版日期:2026-03-28 发布日期:2026-03-31
  • 通讯作者: 王晓茜 E-mail:xiaoqian0103@hotmail.com
  • 基金资助:
    江苏省口腔疾病研究重点实验室开放课题基金(JSKLOD-KF-1908);江苏省预防医学科研课题指导性项目(Yl2023021);江苏省科教能力提升工程——江苏省研究型医院建设单位(YJXYYJSDW4);江苏省医学创新中心(CXZX202227);南通市自然科学基金(JC2025073)

The mechanism of circRNA_3498 inhibiting autophagy in promoting periodontal inflammation in mice with type 2 diabetes mellitus

MEI Youmin1,2, HUANG Lingyan2, SHEN Xiang3, WANG Xinlei4, WANG Xiaoqian1,5()   

  1. State Key Laboratory Cultivation Base of Research, Prevention and Treatment for Oral Diseases, Nanjing 210029, China
  • Received:2024-10-29 Online:2026-03-28 Published:2026-03-31

摘要:

目的 研究circRNA_3498靶向抑制自噬在2型糖尿病(type 2 diabetes mellitus,T2DM)小鼠牙周组织破坏中的作用。方法 提取T2DM患者和健康志愿者的外周血单个核细胞(peripheral blood mononuclear cells,PBMCs),进行转录组测序和生物信息学分析检测circRNA的差异性表达。构建T2DM小鼠模型,免疫组化染色观察T2DM小鼠牙周组织中自噬相关蛋白LC3B和炎症相关蛋白白介素(interleukin,IL)-1β、IL-18表达。提取正常小鼠骨髓来源巨噬细胞(bone marrow-derived macrophages,BMDMs),通过慢病毒和siRNA干扰巨噬细胞circRNA_3498表达,Western blot检测LC3B、CD86、CD206水平,ELISA检测IL-1β、IL-18表达。结果 与健康志愿者相比,circRNA_3498在T2DM患者PBMCs中表达水平明显较高(P<0.05)。在T2DM小鼠牙周组织中,LC3B表达明显降低,IL-1β和IL-18表达均明显增高(P<0.05)。慢病毒干扰BMDMs抑制circRNA_3498表达,LC3-Ⅱ/LC3-Ⅰ值明显下降(P<0.05),CD206阳性表达减少(P<0.05),CD86阳性表达增加(P<0.05),细胞上清液中IL-1β(P<0.01)和IL-18(P<0.05)水平增高;siRNA-circRNA_3498干预抑制circRNA_3498的表达后,上述指标变化相反。结论 circRNA_3498通过靶向抑制自噬相关蛋白促进T2DM小鼠牙周组织炎症反应的发生。

关键词: circRNA_3498, 自噬, 2型糖尿病, 牙周组织, 巨噬细胞

Abstract:

Objective To study the role of circRNA_3498 targeted inhibition of autophagy in the destruction of periodontal tissue in mice with type 2 diabetes mellitus (T2DM). Methods The peripheral blood mononuclear cells from patients with T2DM and healthy volunteers were extracted for transcriptome sequencing and bioinformatics analysis of the differential expression of circRNA. The T2DM mouse model was constructed and the changes of autophagy related protein LC3B, interleukin(IL)-1β and IL-18 in the periodontal tissue structure of mice with T2DM were observed by immunohistochemical staining. Bone marrow-derived macrophages (BMDMs) were isolated from mice. The expression of circRNA_3498 in macrophages was interfered using lentivirus and siRNA. Western blot and ELISA were performed to detect the levels of LC3B, IL-1β, IL-18, as well as macrophage markers CD86 and CD206. Results Compared with the healthy people, circRNA_3498 was highly expressed in PBMCs of patients with T2DM (P<0.05). The expression level of LC3B was reduced in periodontal tissue of mice with T2DM, while IL-1β and IL-18 showed high expression (P<0.05). Lentivirus interference in BMDMs stimulated the expression of circRNA_3498, resulting in a significant decrease in the expression levels of LC3-Ⅱ/LC3-Ⅰ (P<0.05), a reduction in CD206 positive expression (P<0.05), an increase in CD86 positive expression (P<0.05), and an increase in the levels of IL-1β (P<0.01) and IL-18 (P<0.05). After siRNA-circRNA_3498 intervention to inhibit the expression of circRNA_3498, the results were reversed. Conclusion circRNA_3498 promotes inflammation of periodontal tissue by targeting inhibition of autophagy related proteins in mice with T2DM.

Key words: circRNA_3498, autophagy, type 2 diabetes mellitus, periodontal tissue, macrophages

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