RESUMO
Secondary spinal cord injury (SCI) sets on immediately after trauma which results in vascular, morphological and biochemical changes at the site of lesion. Amongst these, the crucial events such as oxidative stress and apoptosis result in spreading the injury to adjacent tissues following the initial insult. Exposure to extremely low frequency magnetic field (ELFMF) is reported to modulate oxidative stress and cell death in vivo. Here, we investigated the influence of ELFMF on oxidative stress and cell death after SCI. Adult male Wistar rats were divided into Sham-SCI (Laminectomy only), Sham-SCI+MF (ELFMF exposure; 17.96 ?T intensity, 50 Hz frequency, 2 h duration/day to Sham-SCI rats), SCI (complete transection of T13 spinal cord) and SCI+MF (ELFMF exposure to SCI rats) groups. They were sacrificed on day 2 for antioxidant assay and day 1, 2 and 3 for cell death study. The oxidative stress was assessed by antioxidant enzyme activities and the cell death was assessed by TUNEL assay and Caspase-3 immnuohistochemistry. Data revealed significant reduction in the lipid peroxidation and number of cells undergone cell death besides improvement in antioxidant levels in the spinal cord of ELFMF exposed SCI rats. These novel findings demonstrate the potential of ELFMF to attenuate oxidative stress and cell death in the early stage of secondary injury process after SCI.
RESUMO
Background:To investigate the effect of chronic exposure to extremely low frequency magnetic field (ELF- MF) on pain modulation status of completely spinal cord injured (SCI) in rats. Methods: Male Wistar rats were divided into Sham (Laminectomy), SCI (complete transection of T13 spinal cord) and SCI+MF (ELF-MF: 17.96 μT, 50 Hz, 2h/day exposure to SCI rats) groups. Pain was studied by utilizing threshold of tail flick (TTF), forepaw lick latency (FPL) and its modulation by temporal summation (TS) and diffuse noxious inhibitory control (DNIC). These tests were performed before surgery (week 0), and after surgery (weeks 4 and 8). Locomotor function was assessed by BBB score at post-SCI weeks 1,3,5,7 and 8. At the end of week 8, spinal cords were collected for histological analysis. Results: Data revealed post-SCI significant decrease in TTF and FPL. The amplitude of TS response was increased, while TTF response was not disappeared after pressure pain application in DNIC paradigm. SCI rats also revealed a significant lower BBB score. However, MF exposure to SCI rats significantly restored the above parameters. Conclusion: Our observations suggested reduction in post-SCI hyperalgesia by inactivation of descending facilitatory system after MF exposure to SCI rats.