The effects of tacrolimus postconditioning on protein-serine-threonine kinases(Akt) phosphorylation and apoptotic cell death in rats after spinal cord ischemia-reperfusion injury were investigated.Ninety male SD rats were randomly divided into sham operation group,ischemia-reperfusion group and tacrolimus postconditioning group.The model of spinal cord ischemia was established by means of catheterization through femoral artery and balloon dilatation.The spinal cord was reperfused 20 min after ischemia via removing saline out of balloon.The corresponding spinal cord segments were excised and determined for Akt activity in spinal cord tissue by using Western blotting at 5,15,and 60min after reperfusion respectively.Spinal cord tissue sections were stained immunohistochemically for detection of the phosphorylated Akt expression at 15 min after reperfusion.Flow cytometry was applied to assess apoptosis of neural cells,and dry-wet weights method was employed to measure water content in spinal cord tissue at 24 h after reperfusion.The results showed that the activities of Akt in tarcolimus postconditioning group were significantly higher than those in ischemia-reperfusion group at 5,15,and60 min after reperfusion(P<0.05,P<0.01).The Akt activities reached the peak at 15 min after reperfusion in ischemia-reperfusion group and tacrolimus postconditioning group.The percentage of apoptotic cells and water content in spinal cord tissue were significantly reduced(P<0.01) in tacrolimus postconditioning group as compared with those in ischemia-reperfusion group at 24 h after reperfusion.It is concluded that tacrolimus postconditioning can increase Akt activity in spinal cord tissue of rats,inhibit apoptosis of neural cells as well as tissue edema,and thereby alleviate spinal cord ischemia-reperfusion injury. The effects of tacrolimus postconditioning on protein-serine-threonine kinases (Akt) phosphorylation and apoptotic cell death in rats after spinal cord ischemia-reperfusion injury were studied. Ninety male SD rats were differentiated into sham operation group, ischemia-reperfusion group and tacrolimus postconditioning group. The model of spinal cord ischemia was established by means of catheterization through femoral artery and balloon dilatation. The spinal cord was reperfused for 20 min after ischemia via removing saline out of balloon. The spinal cord segments were excised and determined for Akt activity in spinal cord tissue by using Western blotting at 5,15, and 60 min after reperfusion respectively. spinal cord sections were stained immunohistochemically for detection of the phosphorylated Akt expression at 15 min after reperfusion. Flow cytometry was applied to assess apoptosis of neural cells, and dry-wet weights method was employed to measure water content in spin al cord tissue at 24 h after reperfusion. The results showed that the activities of Akt in tarcolimus postconditioning group were significantly higher than those in ischemia-reperfusion group at 5,15, and 60 min after reperfusion (P <0.05, P <0.01). The Akt activities reached the peak at 15 min after reperfusion in ischemia-reperfusion group and tacrolimus postconditioning group. Percentage of apoptotic cells and water content in spinal cord tissue were significantly reduced (P <0.01) in tacrolimus postconditioning group as compared with those in ischemia-reperfusion group at 24 h after reperfusion. It is said that tacrolimus postconditioning can increase Akt activity in spinal cord tissue of rats, inhibit apoptosis of neural cells as well as tissue edema, and thereby alleviate spinal cord ischemia-reperfusion injury.