TRIM52 knockdown inhibits proliferation, inflammatory responses and oxidative stress in IL‐1β‐induced synovial fibroblasts to alleviate temporomandibular joint osteoarthritis

Abstract

AbstractTo 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.