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Spinal cord injury (SCI) is one of the most common and serious condition, which leads to permanent neurological dysfunction and poor prognosis in patients. Hyperglycemia impairs neural functional recovery after SCI resulting in the overproduction of reactive oxygen species (ROS) and inflammatory cytokines. However, the effect of glucose metabolism in the spinal cord after injury remains unclear. AKR1B1, one member of the aldo/keto reductase superfamily, is involved in the energy metabolism of plasm glucose and ROS production. The role of AKR1B1 in cancer cell proliferation and invasion has been confirmed. Meanwhile, Akt, one pivotal transcription factor particularly, is involved in the regulation of cell cycle and ROS-mediated secondary injury in the lesion site. In our study, we established an acute SCI rat model to identify the expression of AKR1B1 and its role in neural recovery processes. Western blotting revealed the expression of AKR1B1 protein was elevated after injury, peaked at 3 days and declined gradually to normal at 14 days. Similar results was illustrated in immunohistochemistry staining of white matter. Double immunofluorescence staining showed AKR1B1 was expressed in glial cells and its expression was significantly increased in proliferative astrocytes during the pathological processes. Further experiments showed AKR1B1 was co-located with Akt protein in GFAP positive cells and immunoprecipitated with Akt in injured spinal cord as well. In summary, the present study demonstrated AKR1B1 played a vital role in astrocytes proliferation through Akt pathway, associated with the metabolism of hyperglycemia induced by SCI.