Abstract: OBJECTIVE To investigate the effect of rosiglitazone on intestinal ischemia reperfusion injury and its potential mechanism. METHODS Thirty rats were randomly divided into sham operation group, ischemia reperfusion injury group(IRI group) and IR plus rosiglitazone preconditioning group(RGZ group). RGZ group were administered by intravenous injection (0.3?mg·kg^-1) 60 min prior to operation in RGZ group, and the equal volume of saline was administered in the other 2 groups. The intestinal IR injury was induced in IRI group and RGZ group using bulldog clamps on superior mesenteric artery by 45 min of ischemia followed by 4 h of reperfusion. The pathology of intestinal tissues was observed according to PAS staining. The expression level of IL-6, TNF-α and IFN-γ were measured by PCR and ELISA. The expression of p-PPAR-γ, PPAR-γ, JAK2, p-JAK2, STAT3 and p-STAT3 were measured by Western blot. RESULTS Compared with the sham operation group, the level of mesenteric injuries in IRI group was significantly higher. Moreover, the expression level of IL-6, TNF-α, IFN-γ, p-PPAR-γ, p-JAK2 and p-STAT3 were all higher than the sham operation group, but the expression level of PPAR-γ, JAK2 and STAT3 had no difference. Compared with the IRI group, the level of mesenteric injuries, the expression level of IL-6, TNF-α and IFN-γ in the RGZ group were significantly reduced, but the expression of p-PPAR-γ, p-JAK2 and p-STAT3 were further increased and the expression level of PPAR-g, JAK2 and STAT3 still had no difference between IRI and RGZ groups. CONCLUSION Rosiglitazone preconditioning can protects rats against intestinal ischemia-reperfusion injury by activating JAK2/STAT3 signal pathway to attenuate inflammation.