Co-Culture of Bone Marrow Mesenchymal Stem Cells and Fibroblast-Like Synoviocytes (RA-FLS) Alleviates Rheumatoid Arthritis Cell Apoptosis by Inhibiting Inflammatory Response

Objective: To investigate the effect of bone marrow mesenchymal stem cells (bmsc) on RA-fibroblast-like synovial cells (FLS) and collagen-induced arthritis (CIA), and to further explore the mechanism of action. Methods: The rheumatoid arthritis cell model was established, and the cells were co-cultured with BMSC. The proliferation and apoptosis of the cells were detected by MTT and flow cytometry, the expression level of inflammatory factors in the cells was detected by ELISA, and the phosphorylation activation and expression of proteins in related pathways were analyzed by western blotting. Results: bmsc inhibited the proliferation of TNF-a-induced RA-FLS, increased the apoptosis rate, and up-regulated caspase-3, PARP and Burlington levels. Meanwhile, the expression of il-10, il-1 β and il-6 was inhibited. p-STAT3 levels were down-regulated in a dose-dependent manner. Overexpression of STAT3 partially neutralizes BMSC-mediated caspase-3 increase and PARP shear, as well as down-regulation of il-10, IL-1B, and il-6. This suggests that BMSCs inactivate the STAT3 pathway. In addition, BMSCs can effectively inhibit the production of inflammatory cytokines in rat models of RA-FLS and CIA. Conclusions: In summary, synthesis is a potential long-term treatment drug for rheumatoid arthritis, which can play a therapeutic role in rheumatoid arthritis by inactivating the STAT3 pathway. At the same time, it reveals the role of STAT3 pathway in the pathogenesis of rheumatoid arthritis, and suggests the possibility of STAT3 pathway as a therapeutic target for rheumatoid arthritis.