To analyze the inflammatory level and mechanism of acupuncture and moxibustion in improving knee osteoarthritis(KOA).Methods:Forty SD rats were randomly divided into a sham operation group，a model group，a moxibustion group，and an acupuncture group，with 10 rats in each group.Except for the sham operation group and the model group，the KOA model was established in the other rats by the modified Hulth method.The sham operation group and the model group did not intervene.The moxibustion group and the acupuncture group were treated with moxibustion and acupuncture，respectively，at the Neixiyan，Waixiyan，and Zusanli.The treatment time was 6 min，once a day for 4 weeks.After treatment，the exercise ability of rats in each group was assessed.Enzyme-linked immunosorbent assay(ELISA)，fluorescence quantitative polymerase chain reaction(qPCR)，and Western blotting were used to detect the inflammation levels，brain and muscle aryl hydrocarbon receptor nuclear translocator-like protein 1(Bmal1)，circadian clock gene(Clock)，Toll-like receptor 4(TLR4)，nuclear factor-κB(NF-κB)，as well as the mRNA and protein expression of myeloid differentiation primary response protein 88(MyD88).Results:The gait and claw pressure scores of rats in the model group were higher than those in the sham operation group，while the above scores in the moxibustion group and acupuncture group were lower than those in the model group.The inflammatory mediator levels in the model group were significantly higher than those in the sham operation group.The mRNA and protein expression levels of Bmal1 and Clock were decreased，while those levels of TLR4，NF-κB，and MyD88 were significantly increased，with statistically significant differences(P<0.05).Compared with the model group，relevant indicators were significantly reversed in the moxibustion group and the acupuncture group，with better improvement in the acupuncture group(P<0.05).Conclusion:Acupuncture and moxibustion treatment may reduce the inflammatory mediator levels in KOA and up-regulate the Bmal1 and Clock expression by inhibiting the TLR4/NF-κB signaling pathway，thus alleviating the KOA disease progression.