RESUMO
OBJECTIVE: This experiment explored the function of TTC4 in rheumatoid arthritis inflammation and its possible mechanism. METHODS: C57BL/6 mice were immunized intradermally with bovine type II collagen. Lipopolysaccharide induction was performed on RAW264.7 cells. RESULTS: The mRNA expression of TTC4 in articular tissue of mice with rheumatoid arthritis was downregulated. Sh-TTC4 virus increased arthritis score, morphological change score, paw edema, and spleen index, as well as alkaline phosphatase level in mice with rheumatoid arthritis. Sh-TTC4 virus increased the levels of inflammatory factors and MDA, and decreased anti-oxidant factors in articular tissue of mice with rheumatoid arthritis. TTC4 reduced inflammation and oxidative stress in an in vitro model. TTC4 regulated HSP70 in a rheumatoid arthritis model. The inhibition of HSP70 reduced the effects of sh-TTC4 gene in mice with rheumatoid arthritis. METTL3 reduced the stability of the TTC4 gene. CONCLUSION: In this study, the TTC4 gene reduced oxidative response and inflammation in the rheumatoid arthritis model through the HSP70/NLRP3 pathway. Therefore, it can be concluded that TTC4 can be used as diagnosis and prognosis evaluation of rheumatoid arthritis.
