No abstract

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. Rats were divided into one sham group and six with TSCI; one of them received no treatment, and the rest were treated with NDC, MP, NDC + MP, NDC + ANT or ANT. The ANT group decreased lactate and creatine phosphokinase levels and increased the amount of preserved tissue (morphometric analysis) as well as functional recovery (Basso, Beattie and Bresnahan or BBB motor scale). In contrast, NDC treatment increased lipid peroxidation, measured through thiobarbituric acid reactive substances (TBARS) levels, as well as spinal cord tissue destruction and functional deficit. Early metabolic reactivation after a TSCI may be deleterious, while natural early metabolic inhibition may not be a "secondary mechanism of injury" but a "secondary neuroprotective response". While increased antioxidant defence after a TSCI may currently be an ideal therapeutic strategy, the usefulness of metabolic reactivation should be tested in the sub-acute or chronic phases of TSCI and new strategies must continue to be tested for the early ones.

No abstract

Genes regulated by NF‐κB 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‐κB, pyrrolidine dithiocarbamate (PDTC) or lipopolysaccharide were given to rats before or after SC contusion. The amount of spared SC tissue was higher (P < 0.05) at 24 h postinjury in rats posttreated with PDTC; both PDTC‐treated rats showed no significant trend to decrease polymorphonuclear infiltrate. p65 subunit was present in inflammatory cells, neurons, and astrocytes at the injury site. These data support further investigation on functional effects of NF‐κB inhibition in acute SCI.

SUMMARYTraumatic spinal cord injury (TSCI) produces paralysis by destruction of axons and demyelination of surviving fibers. Using methylprednisolone (MP) as neuroprotector and a predegenerated peripheral nerve (PPN) graft as regenerative strategy, 83 rats with TSCI were divided into nongrafted, fresh peripheral nerve (FPN) and PPN grafted groups with and without MP administration. Myelination index (MI), number of axons, myelinated fibers, and axon collaterals were assessed 21 h, 7 days, 2, and 4 months after TSCI. Animals with PPN grafts showed more axons and myelinated fibers than animals with FPN grafts, while the latter showed the highest number of axon collaterals. When MP was used, collateral emission was decreased in all treated groups. However, PPN graft plus MP group had the best MI and highest number of axons and myelinated fibers. Combination of one neuroprotective with a regenerative strategy is a good therapeutic option, although new combinations should be f?&her explored.