Objective:To investigate the role and mechanism of G-protein-coupled receptor kinase interacting protein 1(GIT1) and Extracellular signal-regulated kinases 1 and 2(ERK1/2) in reperfusion of ischemic spinal cord. Methods:The morphology of spinal cord was observed by electron microscope in different time courses after ischemia/reperfusion injury[group A(control group),group B(ischemia 30 min/reperfusion 30 min),group C(ischemia 30 min/reperfusion 2 h),group D(ischemia 30 min/reperfusion 8 h)]. The phosphorylation of ERK1/2 and GIT1 was detected by Western blot. The interaction between GIT1 and pERK1/2 was detected by coimmunoprecipitation. The localization of pERK1/2 was analyzed by immunohistochemistry. Results:The apoptosis of neurocytes of spinal cord undergoing ischemia/reperfusion injury in group D was detected by electronmicroscope. The phosphorylation of ERK1/2 and GIT1 and the interaction between GIT1 and pERK1/2 significantly increased in group C and D. Immunohistochemistry results showed that the stagnation of pERK1/2 was observed in the cytoplasma of neurocytes in group C and D. Conclusion:The stagnation of pERK1/2 in the cytoplasm might act as apoptosis signals contributing to the apoptosis of neurocytes of spinal cord after ischemia/reperfusion injury,and the interaction between GIT1 and pERK1/2 might cause the stagnation of pERK1/2 in the cytoplasm of neurocytes.