OBJECTIVE： To study the protective effect of fingolimod on renal ischemia reperfusion injury （RIRI） model mice and its mechanism. METHODS： A total of 60 mice were randomly divided into sham operation group， model group， fingolimod group （1 mg/kg） and fingolimod+wortmannin group [fingolimod 1 mg/kg+phosphatidylinositol 3-kinase （PI3K） specific blocker wortmannin 1.4 mg/kg]， with 15 mice in each group. Except for sham operation group， RIRI model was induced in other 3 groups， and those model mice were given relevant medicine via caudal vein at once 24 h before surgery. Serum of mice were collected in each group after 24 h perfusion. Serum levels of Scr and BUN were measured by automatic biochemical analyzer. The pathological changes of renal tissue were observed under light microscope. The protein expression of intercellular cell adhesion molecule-1 （ICAM-1）， monocyte chemoattractant protein-1（MCP-1） and phosphorylated protein kinase B （p-Akt） in renal tissue were measured by Western blot assay. RESULTS： Compared with sham operation group， the serum levels of Scr and BUN in model group were increased significantly （P＜0.01）. Pathological changes were found in the kidney， and RIRI led to widespread renal tubular epithelial cell injury， apoptosis and inflammatory cells infiltration. The protein expression of ICAM-1 and MCP-1 in renal tissue were increased significantly （P＜0.01）， the protein expression of p-Akt was increased slightly （P＞0.05）. Compared with mo- del group， other indexes of fingolimod group were improved significantly （P＜0.01） except that the protein expression of p-Akt in renal tissue was increased significantly （P＜0.01）. Compared with fingolimod group， above indexes of fingolimod+wortmannin group were reversed （P＜0.05 or P＜0.01）. CONCLUSIONS： Fingolimod can obviously ameliorate renal injury induced by RIRI in mice， the mechanism of which may be associated with the activation of PI3K/Akt signaling pathway.