Influence Of CXCL13 On The Expressions Of Rankl In Osteoarthritis HS Cells

Objective:To investigate the effect of CXCL13 on the expression of RANKL in synoviocytes of osteoarthritis and to explore the correlation between CXCL13 and osteoarthritis in synoviocytes of osteoarthritis.Methods:The synovial cell model of synovial cells was established by treating normal synovial cells with TNF-?,an inflammatory cytokine approved by the academic community.The expression and distribution of CXCL13 were detected by immnofluorescence(IF)and confocal laser scanning microscopy.The chemotactic factor CXCL13 was further used to treat synovial cell inflammation model.The expression of RANKL protein in the synoviocyte inflammatory model treated with CXCL13(under different concentration and different time)was detected by Western Blot.Results:Immunofluorescence results showed that the expression of CXCL13 in synovial cells of osteoarthritis was significantly lower than that of normal human synovial cells.The expression of CXC113 decreased with the prolongation of the time of treatment of normal synovial cells with TNF-?(concentration of lOug/L).The expression of RANKL protein in synovial cells of osteoarthritis was significantly higher than that of normal human synovial cells.After treatment with TNF-?(concentration of 10ng/ml)for 24 hours,the expression of CXCL13(25 ng/ml),the expression level of RANKL protein in osteoarthritis synovial cells was decreased after 3 h,3 h,6 h and 24 h.After treated with TNF-?(concentration of 10 ng/ml)for 24 h,the culture medium containing different concentrations of chemokine CXCL13(Ong/ml,5ng/ml,15ng/ml,25ng/ml)The expression level of RANKL protein decreased with the increase of concentration.The protein expression of RANKL in synovial cells of osteoarthritis increased with time and the time-dependent and concentration-dependent decrease of CXC113 stimulation.Conclusion:CXCL13 can inhibit the expression of RANKL at a certain concentration and time,which may further delay the progression of inflammation,bone destruction and cartilage sclerosis of osteoarthritis.