AI Article Synopsis
- Secondary tissue damage after spinal cord injury can lead to permanent paralysis and other disabilities, largely due to acute inflammation.
- Administering 15-deoxy-delta-12,14-prostaglandin J2 (15d-PGJ2), an anti-inflammatory metabolite, during the first two weeks post-injury significantly improves sensory and locomotor functions in mice.
- The treatment decreases inflammation, shown by reduced microglia/macrophage activity, increased neuron survival, and lower levels of pro-inflammatory molecules, by modulating various signaling pathways.
Article Abstract
Secondary tissue damage that occurs within days after spinal cord injury contributes significantly to permanent paralysis, sensory loss, and other functional disabilities. The acute inflammatory response is thought to contribute largely to this secondary damage. We show here that 15-deoxy-delta-12,14-prostaglandin J2 (15d-PGJ2), a metabolite of prostaglandin D2 (PGD2) that has anti-inflammatory actions, given daily for the first 2 weeks after spinal cord contusion injury in mice, results in significant improvement of sensory and locomotor function. 15d-PGJ2-treated mice also show diminished signs of microglia/macrophage activation, increased neuronal survival, greater serotonergic innervation, and reduced demyelination in the injured spinal cord. These changes are accompanied by a reduction in chemokine and pro-inflammatory cytokine expression. Our results also indicate that 15d-PGJ2 is likely to reduce inflammation in the injured spinal cord by attenuating multiple signaling pathways: reducing activation of NF-kappa B; enhancing expression of suppressor of cytokine signaling1 and reducing the activation of Janus activated Kinase 2.
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| http://dx.doi.org/10.1002/glia.20630 | DOI Listing |
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