OBJECTIVE： To investigate the anti-inflammatory effects of liensinine on 12-O-tetradecanoylphorbol-13-acetate （TPA）-induced ear edema inflammatory model mice， and to investigate its mechanism. METHODS： The 40 mice were randomly divided into blank group， model group， positive control group （dexamethasone， 2.5 mg/kg） and liensinine low-dose and high-dose groups （5， 15 mg/kg）， with 8 mice in each group. Except for blank group， other groups were given TPA for external use on both inner and outer sides of right ear to induce ear edema inflammatory model. During modeling， administration group was given relevant medicine 20 μL/mice for external use on both inner and outer sides of right ear （using acetone as solvent）； blank group and model group were given constant volume of acetone. 6 h after administration， ear thickness and ear edema degree of mice were determined. The pathological changes of ear tissue were observed by HE staining. The levels of inflammatory factors （TNF-α， IL-6， IL-1β） in ear tissue were detected by ELISA. The phosphorylation levels of nuclear factor κB （NF-κB） signaling pathway related protein [NF-κB p65， NF-κB inhibitory protein （IκBα）] were detected by Western blot assay. mRNA expressions of COX-2 and iNOS were detected by RT-PCR. RESULTS： Compared with blank group， degree of ear edema， the levels of inflammatory factors in ear tissue， phosphorylation levels of NF-κB signaling pathway related protein， mRNA expressions of COX-2 and iNOS were increased significantly （P＜0.05）. There were ear tissue thickening and increase of inflammatory cell infiltration， etc. Compared with model group， ear edema degree and above indexes of ear tissue in administration group were decreased significantly （P＜0.05）； ear tissue thickening and increase of inflammatory cell infiltration were relieved significantly. CONCLUSIONS： Liensinine shows good anti-inflammatory effects on TPA-induced ear edema inflammatory model mice， the mechanism of which may be associated with inhibiting the phosphorylation levels of NF-κB p65 and NF-κB protein and inhibiting the mRNA expressions of inflammatory factors COX-2 and iNOS.