To explore the mechanism of tripartite motif 52 (TRIM52) in the progression of temporomandibular joint osteoarthritis (TMJOA). Gene and protein expression were tested by quantitative real‐time polymerase chain reaction and western blot, respectively. The levels of pro‐inflammatory cytokines and oxidative stress factors were evaluated using enzyme‐linked immunosorbent assay and biochemical kit, respectively. Cell counting kit‐8 and 5‐ethynyl‐2′‐deoxyuridine assays were carried out to assess cell proliferation. Immunofluorescence was used to detect the expression of CD68 and Vimentin in primary synovial fibroblasts (SFs). Haematoxylin and eosin staining and Safranin O/Fast green were used to evaluate the pathological damage of synovial and cartilage tissue in rats. TRIM52 was upregulated in the synovial tissue and SFs in patients with TMJOA. Interleukin (IL)‐1β treatment upregulated TRIM52 expression in TMJOA SFs and normal SF (NSF), promoting cell proliferation, inflammatory response and oxidative stress in NSF, SFs. Silence of TRIM52 relieved the cell proliferation, inflammatory response and oxidative stress induced by IL‐1β in SFs, while overexpression of TRIM52 enhanced IL‐1β induction. Meanwhile, IL‐1β induction activated toll‐like receptor 4 (TLR4)/nuclear factor (NF)‐κB pathway, which was augmented by upregulation of TRIM52 in NSF, and was attenuated by TRIM52 knockdown in SFs. Besides, pyrrolidinedithiocarbamic acid ameliorated IL‐1β‐induced proliferation and inflammatory response by inhibiting TLR4/NF‐κB signalling. Meanwhile, TRIM52 knockdown inhibited cell proliferation, oxidative stress and inflammatory response in IL‐1β‐induced SFs through downregulation of TLR4. TRIM52 promoted cell proliferation, inflammatory response, and oxidative stress in IL‐1β‐induced SFs. The above functions were mediated by the activation of TLR4/NF‐ κB signal pathway.

中文翻译：

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TRIM52 敲低抑制 IL-1β 诱导的滑膜成纤维细胞的增殖、炎症反应和氧化应激，以减轻颞下颌关节骨关节炎

探讨三联基序52（TRIM52）在颞下颌关节骨关节炎（TMJOA）进展中的机制。分别通过定量实时聚合酶链反应和蛋白质印迹测试基因和蛋白质表达。分别使用酶联免疫吸附测定和生化试剂盒评估促炎细胞因子和氧化应激因子的水平。进行细胞计数试剂盒-8和5-乙炔基-2'-脱氧尿苷测定以评估细胞增殖。免疫荧光法检测原代滑膜成纤维细胞（SF）中CD68和Vimentin的表达。采用苏木精-伊红染色和番红O/固绿评价大鼠滑膜和软骨组织的病理损伤。 TRIM52 在 TMJOA 患者的滑膜组织和 SF 中表达上调。白细胞介素 (IL)-1β 治疗上调 TMJOA SF 和正常 SF (NSF) 中 TRIM52 的表达，促进 NSF、SF 中的细胞增殖、炎症反应和氧化应激。 TRIM52 的沉默减轻了 SF 中 IL-1β 诱导的细胞增殖、炎症反应和氧化应激，而 TRIM52 的过表达则增强了 IL-1β 的诱导。同时，IL-1β诱导激活了Toll样受体4（TLR4）/核因子（NF）-κB通路，该通路通过NSF中TRIM52的上调而增强，并通过SF中TRIM52的敲低而减弱。此外，吡咯烷二硫代氨基甲酸通过抑制 TLR4/NF-κB 信号传导改善 IL-1β 诱导的增殖和炎症反应。同时，TRIM52 敲低通过下调 TLR4 抑制 IL-1β 诱导的 SF 中的细胞增殖、氧化应激和炎症反应。 TRIM52 促进 IL-1β 诱导的 SF 中的细胞增殖、炎症反应和氧化应激。上述功能是通过TLR4/NF-κB信号通路的激活介导的。