基于CX3CL1/NF-κB信号通路探讨补肾强督方抑制M1巨噬细胞极化治疗强直性脊柱炎的机制研究OA北大核心CSTPCD

Objective:To observe the effect of Bushen Qiangdu formula on CX3CL1/NF-κB signaling pathway mediated po-larization of M1 macrophages and elucidate its molecular mechanism in treating ankylosing spondylitis.Methods:Lipopolysaccha-ride(LPS)-induced THP-1 cells were used to construct a cell model,and Bushen Qiangdu medicated serum and CX3CL1 inhibi-tor AZD8797 were given for intervention.The levels of inflammatory factors(TNF-α,IL-6,IL-1β and IL-17)were detected by enzyme-linked immunosorbent assay.CD86 expression was detected by flow cytometry.Expression of iNOS,osteoblast differenti-ation marker proteins(TRAP,calcitonin and p-NFATC1β)and the CX3CL1/NF-κB pathway was assessed by Western blot.The expression of iNOS mRNA was quantified by real-time quantitative polymerase chain reaction(qRT-PCR).Results:Com-pared with the control group,the content of TNF-α,IL-6,IL-1β,IL-17 in macrophages and the proportion of CD86+macro-phages in the model group were significantly increased,and iNOS,CX3CL1,p-P65,p-IkKα/β,p-IkBα,TRAP,calcitonin and p-NFATC1β protein and iNOS mRNA expression were significantly upregulated,all of which were statistically significant(P<0.01).Bushen Qiangdu-medicated serum significantly decreased the content of TNF-α,IL-6,IL-1β,IL-17 and the proportion of CD86+macrophages,and down-regulated the expression of iNOS,CX3CL1,p-P65,p-IKKα/β,p-IkBα,TRAP,Calcitonin and p-NFATC1β proteins and iNOS mRNA expression,which showed statistically significant differences compared with the model group(P<0.05).Conclusion:Bushen Qiangdu formula inhibits M1 polarization of macrophages by inhibiting CX3CL1/NF-κB signaling pathway,then playing a role of inhibiting inflammation and osteoclast differentiation in the treatment of ankylosing spon-dylitis.