To explore the mechanism by which Danshensu protects against hypoxia-induced injury in fibroblast-like synovial cells.Methods:Rat fibroblast-like synovial cells were randomly divided into control,hypoxia,low-dose,medium-dose,and high-dose groups.The effect of Danshensu on fibroblast-like synovial cells were observed.Additionally,cells from the same generation of rats were divided into control,hypoxia,high-dose,and BAY11-7082 groups to assess the effect of the NF-κB p65 inhibitor BAY11-7082 on fibroblast-like synovial cell injury.Cell proliferation was detected by 5-ethynyl-2'-deoxyuridine(Edu) assay,protein expression levels were analyzed using Western blot,and mRNA expression of matrix metalloproteinases(MMPs) and vascular endothelial growth factor(VEGF) was measured by RT-qPCR.Results:In the hypoxia group,Edu-positive cell rate,Ki67,CyclinD1 protein expression,MMP-1,MMP-9,MMP-3,VEGF mRNA,and phosphorylated(p)-NF-κB p65,hypoxia-inducible factor 1α(HIF-1α),interleukin-6(IL-6),and IL-8 protein levels were higher than the control group.Compared with the hypoxia group,low,medium,and high-dose groups showed significantly reduced Edu-positive cell rates,Ki67,PCNA,CyclinD1 protein expression,MMP-1,MMP-9,MMP-3,VEGF mRNA,p-NF-κB p65,HIF-1α,IL-6,and IL-8 protein expression(P<0.05).Compared to the high-dose group,BAY11-7082 treatment further decreased the expression of p-NF-κB p65,HIF-1α,IL-6,IL-8,Edu-positive cell rate,and MMP and VEGF mRNA levels(P<0.05).Conclusion:Danshensu may alleviate hypoxia-induced fibroblast-like synovial cell injury in rats by inhibiting the NF-κB/HIF-1α signaling pathway. |