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Lesion in spinal cord causes a cascade of events such as the apoptosis of neurons and eventually, neurological dysfunction. Neurologic damage developing after acute spinal cord injury is also related with necrosis and free radical formation. Allopurinol, a xanthine oxidase inhibitor, was shown to have protective effects in several studies. B-cell lymphoma 2 (Bcl-2) family proteins regulate apoptosis. Apoptosis causes the death of neuronal cells, particularly neurons and oligodendrocytes in the spinal cord after lesion. Glial fibrillary acidic protein (GFAP) takes part in astrocyte and neuronal interconnection and synaptic transmission.

Neuroprotective effects of allopurinol on spinal cord injury in rats: a biochemical and immunohistochemical study