上海口腔医学 ›› 2022, Vol. 31 ›› Issue (1): 12-16.doi: 10.19439/j.sjos.2022.01.003

• 论著 • 上一篇    下一篇

微小RNA-100-5p对颞下颌关节炎中雷帕霉素靶蛋白的作用机制研究

万志群1, 周正根1, 王竞1, 周群2   

  1. 1.江西省吉安市中心人民医院 口腔科,江西 吉安 343000;
    2.南昌大学第一附属医院 口腔科,江西 南昌 330006
  • 收稿日期:2020-12-02 修回日期:2021-01-12 出版日期:2022-02-25 发布日期:2022-03-10
  • 通讯作者: 万志群,E-mail:ech898@126.com
  • 作者简介:万志群(1967-),男,本科,副主任医师
  • 基金资助:
    国家自然科学基金青年科学基金项目 (31801271)

Mechanism of microRNA-100-5p on mammalian target of rapamycin in temporomandibular arthritis

WAN Zhi-qun1, ZHOU Zheng-gen1, WANG Jing1, ZHOU Qun2   

  1. 1. Department of Stomatology, Ji'an Central People's Hospital of Jiangxi Province. Ji'an 343000;
    2. Department of Stomatology, The First Affiliated Hospital of Nanchang University. Nanchang 330006, Jiangxi Province, China
  • Received:2020-12-02 Revised:2021-01-12 Online:2022-02-25 Published:2022-03-10

摘要: 目的: 探讨微小RNA-100-5p(miR-100-5p)对颞下颌关节炎中雷帕霉素靶蛋白(mTOR)的作用机制。方法: 60只SD大鼠随机分为A组、B组、C组、D组和E组,每组12只,向双侧颞下颌关节腔内注射碘乙酸钠溶液,制备颞下颌关节炎大鼠模型。造模成功后,C组注射pcDNA3.1-miR-100-5p重组质粒,D组注射mTOR抑制剂雷帕霉素(rapamycin),E组注射pcDNA3.1-miR-100-5p重组质粒和rapamycin,A组注射等剂量生理盐水,比较各组大鼠颞下颌关节组织形态学变化,颞下颌关节组织中基质金属蛋白酶(MMP)-3、MMP-1、MMP-13、白细胞介素1β(IL-1β)、肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)水平及miR-100-5p、mTOR表达量。采用SPSS 22.0软件包对数据进行统计学分析。结果: B组颞下颌关节结构模糊,出现滑膜增生、血管扩张、簇集样细胞团及大量炎症浸润现象,各干预组颞下颌关节组织病理学变化较B组均有不同程度改善,其中,E组改善最明显。B组MMP-3、MMP-1、MMP-13、IL-6、IL-1β、TNF-α水平较A组高(P<0.05);C组、D组、E组MMP-3、MMP-1、MMP-13、IL-6、IL-1β、TNF-α水平较B组低(P<0.05);D组MMP-3、MMP-1、MMP-13、IL-6、IL-1β、TNF-α水平与C组相比差异无统计学意义(P>0.05);E组MMP-3、MMP-1、MMP-13、IL-6、IL-1β、TNF-α水平较D组低(P<0.05);E组miR-100-5p表达量较B组高(P<0.05);E组mTOR蛋白表达量较B组低(P<0.05)。结论: 微小RNA-100-5p可能通过下调雷帕霉素靶蛋白表达而缓解颞下颌关节炎症。

关键词: 微小RNA-100-5p, 雷帕霉素靶蛋白, 颞下颌关节炎, 组织形态学, 基质金属蛋白酶, 炎症因子

Abstract: PURPOSE: To investigate the mechanism of microRNA-100-5p (miR-100-5p) on mammalian target (mTOR) of rapamycin in temporomandibular arthritis. METHODS: Sixty SD rats were randomly divided into group A, group B, group C, group D, and group E, with 12 rats in each group. Rat models of temporomandibular arthritis were prepared by injecting sodium iodoacetate solution into the bilateral spaces of temporomandibular joint. After establishment, group C was injected pcDNA3.1-miR-100-5p recombinant plasmid, group D was injected mTOR inhibitor rapamycin, group E was injected with pcDNA3.1-miR-100-5p recombinant plasmid and rapamycin, and group A was injected same amount of normal saline in the same way. Various indexes were observed in each group, including morphological changes of temporomandibular joint tissues, matrix metalloproteinase-3 (MMP-3), MMP-1, MMP-13, interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), miR-100-5p, mTOR expression. The data were processed using SPSS 22.0 software package. RESULTS: In group B, the structure of temporomandibular joint was fuzzy, with synovial hyperplasia, vascular dilatation, clustered cells and a large amount of inflammatory infiltration. Histopathological changes of temporomandibular joint in each interventional group were improved to different degrees compared with group B, among which group E showed the most obvious improvement. The levels of MMP-3, MMP-1, MMP-13, IL-6, IL-1β and TNF-α in group B were significantly higher than those in group A(P<0.05). The levels of MMP-3, MMP-1, MMP-13, IL-6, IL-1β and TNF-α in group C, group D and group E were significantly lower than those in group B(P<0.05). The levels of MMP-3, MMP-1, MMP-13, IL-6, IL-1β and TNF-α in group D were not significantly different from those in group C (P<0.05). The levels of MMP-3, MMP-1, MMP-13, IL-6, IL-1β and TNF-α in group E were significantly lower than those in group D (P<0.05). The expression level of miR-100-5p in group E was significantly higher than that in group B (P<0.05). The expression level of mTOR protein in group E was significantly lower than that in group B (P<0.05). CONCLUSIONS: MicroRNA-100-5p may alleviate temporomandibular arthritis by down-regulating the expression of mTOR.

Key words: MicroRNA-100-5p, Mammalian target of rapamycin, Temporomandibular arthritis, Histomorphology, Matrix metalloproteinase, Inflammatory factor

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