Objective：To study the therapeutic effect of emodin on inflammatory pain induced by complete Freund’s adjuvant (CFA)in mice and its possible molecular mechanism. Methods：CFA was injected subcutaneously on the dorsal side of the right hind paw of C57BL/6 to induce an inflammatory pain model，and emodin solution was injected intraperitoneally for intervention. The pain threshold was evaluated by the von Frey test and the hot plate test. qRT-PCR and ELISA measure the expression of inflammatory cytokines tumor necrosis factor α(TNF -α)，interleukin -1β(IL -1β)and interleukin -6(IL -6). Western blot was used to detect the expression of transient receptor potential vanillic acid 1(TRPV1)and transient receptor potential vanillic acid 4(TRPV4)in dorsal root ganglion(DRG). Results：The mechanical pain and thermal pain thresholds of mice in the CFA group were significantly lower than those of the control group(P ＜ 0.05). Emodin treatment significantly increased mechanical pain and thermal pain threshold in mice with induced inflammatory pain(P ＜ 0.05). Compared with the control group，emodin intervention can not only significantly reduce the inflammatory cytokines TNF-α，IL-1β and IL-6 in DRG and serum of mice with CFA inflammatory pain，but also reduce the expression levels of TRPV1 and TRPV4 in DRG(P ＜ 0.05). Conclusion：Emodin relieves CFA-induced inflammatory pain by reducing the content of inflammatory cytokines TNF-α，IL-1β and IL-6 in DRG and serum，and down-regulating the expression of pain- related ion channels TRPV1 and TRPV4 in DRG.