Disability after traumatic spinal cord injury (TSCI) results from physical trauma and from "secondary mechanisms of injury" such as low metabolic energy levels, oxidative damage and lipid peroxidation. In order to prove if early metabolic reactivation is a better therapeutic option than antioxidant therapy in the acute phase of TSCI, spinal cord contusions were performed in adult rats using a well-characterized weight drop technique at thoracic 9 level. After TSCI, pyrophosphate of thiamine or non-degradable cocarboxylase (NDC) enzyme was used to maintain energy levels, antioxidants such as superoxide dismutase and catalase (ANT) were used to decrease oxidative damage and methylprednisolone (MP), which has both therapeutic properties, was used as a control.
View Article and Find Full Text PDFGenes regulated by NF-kappaB play an important role on secondary damage and repair after spinal cord injury (SCI). To assess the early effects of the pharmacological inhibition and overactivation of NF-kappaB, pyrrolidine dithiocarbamate (PDTC) or lipopolysaccharide were given to rats before or after SC contusion. The amount of spared SC tissue was higher (P < 0.
View Article and Find Full Text PDFIn the absence of effective regeneration following spinal cord (SC) injury, sprouting from undamaged axons has been regarded as an underlying factor for functional improvement after incomplete SC injury. The influence of spontaneous and induced axonal sprouting at the injury site on motor function was tested using rats subjected to moderate SC contusion at T9 level, using megadoses of methylprednisolone (MP) and intralesion implantation of cells from sciatic nerve (PNI). Groups using MP and PNI combined, implant vehicle, and injury with no treatment were also included.
View Article and Find Full Text PDF