To explore the action mechanism of moxibustion in treating Crohn′s disease (CD)，by observing the effect of herb-partitioned moxibustion on the expressions of NF-κB p65，TNF –α，and IL-1β.Methods:Male Sprague Dawley (SD) rats of clean conventional grade were randomized into four groups，i.e.a normal control (NC) group，a model control (MC) group，a herb-partitioned moxibustion (HPM) group，and a Western medication (WM) group.The CD rat models were developed by using the mixture of 2，4，6 trinitrobenzene sulfonic acid (TNBS) and alcohol via enema.When the models were successfully developed，the HPM group received HPM intervention at bilateral Tianshu (ST 25) and Qihai (CV 6)，and the WM group received Mesalazine via intragastric administration.At the end of treatment，the histopathological variations of rats′ colons were observed by adopting HE staining and light microscope，and the expressions of NF-κB p65，TNF –α，and IL-1β in rats′ colons were determined by using immunohistochemical technique，and the images were all analyzed.Results:Compared to the NC group，the MC group had its rats′ colons present with fissured ulcers and inflammation，and granulomas in submucosa of some colons，and its expressions of NF-κB p65，TNF –α，and IL-1β increased significantly (P<0.01); compared to the MC group，the HPM group and WM group both had rats′ colons present with improved structures and reduced intestinal inflammation，and their expressions of NF-κB p65，TNF –α，and IL-1β dropped significantly (P<0.01); the relevance analyses showed that the expressions of TNF –α and IL-1β both had a positive correlation with the expression of NF-κB p65.Conclusion:HPM can down-regulate the expressions of NF-κB p65，TNF –α，and IL-1β in CD rats′ colons; it′s possible that moxibustion (HPM) produces its therapeutic efficacy by inhibiting the expression of NF-κB p65 in rat′s colon，and subsequently decreasing the expressions of its downstream inflammatory factors，i.e.TNF –α and IL-1β，by which，the intestinal inflammation is relieved and the morphology of colon is improved.