Warming moxibustion attenuates inflammation and cartilage degradation in experimental rabbit knee osteoarthritis

OBJECTIVE:To explore the molecular mechanism of warming moxibustion(WM)in knee osteoarthritis(KOA).METHODS:The knee joints of 40 New Zealand rabbits were placed in a plaster cast in an extended position to establish a KOA model.The animals were randomly divided into four groups:the control group,model group,WM group,and diclofenac(DF)group.Hematoxylin-eosin staining and the modified Mankin score were applied to evaluate the histopathological changes.Chondrocyte apoptosis was determined by the terminal deoxynucleotidyl transferase dUTP nick end labeling(TUNEL)assay.Western blotting and real-time quantitative polymerase chain reaction were performed to measure the expression of interleukin-1β(IL-1β),prostaglandin E receptor 3(PTGER3),a disintegrin-like and metalloproteinase with thrombospondin type-1 motifs-5(ADAMTS-5),matrix metalloproteinase-13(MMP-13),and C-terminal telopeptides of collagen typeⅡ(CTX-Ⅱ)in cartilage tissues of the different groups.The concentrations of IL-1β,PTGER3,and CTX-Ⅱin serum were detected by the enzyme-linked immunosorbent assay.RESULTS:Rabbits with KOA in the WM and DF groups showed significantly reduced cartilage erosion and Mankin scores,compared with the untreated rabbits.The number of TUNEL-positive cells observed in the WM group was much fewer than that in the model group.The expression of PTGER3,MMP-13,CTX-Ⅱ,IL-1β,and ADAMTS-5 in cartilage tissues was remarkably downregulated following therapy with WM and DF.Moreover,a marked reduction was observed in the serum levels of IL-1β,PTGER3,and CTX-Ⅱin the WM and DF groups.CONCLUSION:WM exerts favorable therapeutic effects on articular injuries of KOA by regulating the expression of inflammatory and cartilage degradation-related cytokines.