OBJECTIVE： To study the pharmacodynamic effects of volatile oil from Homalomena occulta on adjuvant-induced arthritis （AA） model rats and its mechanism. METHODS： 60 rats were randomly divided into normal control group （0.5％ polysorbate 80）， model control group （0.5％ polysorbate 80）， positive control group （Tripterygium glycosides tablets， 10 mg/kg）， high-dose， middle-dose and low-dose （0.08， 0.04 and 0.02 ml/kg） groups of volatile oil from H. occulta. Except for normal control group， other groups were given complete Freund’s adjuvant subcutaneously via right rear foot plantar to induce AA model， and given relevant medicine intragastrically for 25 days， once a day， since modeling. The articular swelling degree， immune organ （thymus gland and spleen） index， pathological change， the contents of IL-1β and TNF-α in serum were detected. RESULTS： Compared with normal control group， the primary and secondary articular swelling degree and thymus gland index of rats and the serum contents of IL-1β and TNF-α increased in model control group， while spleen index decreased （P＜0.05 or P＜0.01）； obvious tissue swelling， large amount of neutrophile granulocyte， leukomonocyte and macrophage infiltrating joint surrounding tissue， the proliferation of synovial cells and obvious osteoarthritic lesion were observed in podarthrum. Compared with model control group， the primary and secondary articular swelling degree and  the serum content of IL-1β decreased in the volatile oil from H. occulta groups； thymus gland index increased in middle-dose and low-dose groups of the volatile oil from H. occulta； the content of TNF-α decreased in high-dose group of the volatile oil from H. occulta （P＜0.05 or P＜0.01）. The inflammatory cell infiltration of joint surrounding tissue relieved in treatment groups， synovial cells proliferation was not obvious and synovial cells morphology was improved. CONCLUSIONS： The volatile oil from H. occulta has the pharmacodynamic effects on AA in rat， and its mechanism might be related to the serum content reduction of IL-1β and TNF-α.