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[微小RNA-100-5p在颞下颌关节炎中对雷帕霉素哺乳动物靶点的作用机制]

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

作者信息

Wan Zhi-Qun, Zhou Zheng-Gen, Wang Jing, Zhou Qun

机构信息

Department of Stomatology, Ji'an Central People's Hospital of Jiangxi Province. Ji'an 343000, China. E-mail:

出版信息

Shanghai Kou Qiang Yi Xue. 2022 Feb;31(1):12-16.

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.

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哺乳动物靶点(mTOR)的作用机制。

方法

将60只SD大鼠随机分为A、B、C、D、E组,每组12只。通过向双侧颞下颌关节间隙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,E组注射pcDNA3.1-miR-100-5p重组质粒和雷帕霉素,A组以同样方式注射等量生理盐水。观察各组颞下颌关节组织形态学变化、基质金属蛋白酶-3(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)、miR-100-5p、mTOR表达等各项指标。数据采用SPSS 22.0软件包进行处理。

结果

B组颞下颌关节结构模糊,滑膜增生,血管扩张,细胞聚集,大量炎症浸润。各干预组颞下颌关节组织病理学变化与B组相比均有不同程度改善,其中E组改善最为明显。B组MMP-3、MMP-1、MMP-13、IL-6、IL-1β和TNF-α水平显著高于A组(P<0.05)。C组、D组和E组MMP-3、MMP-1、MMP-13、IL-6、IL-1β和TNF-α水平显著低于B组(P<0.05)。D组MMP-3、MMP-1、MMP-13、IL-6、IL-1β和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和TNF-α水平显著低于D组(P<0.05)。E组miR-100-5p表达水平显著高于B组(P<0.05)。E组mTOR蛋白表达水平显著低于B组(P<0.05)。

结论

微小RNA-100-5p可能通过下调mTOR表达减轻颞下颌关节炎。

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