Object. Because of toxicity at high concentrations, nitric oxide (NO) contributes to spinal cord injury (SCI) secondary lesions. At low concentrations NO modulates nuclear factor-κB (NF-κB) activation. The authors investigated the activity of neuronal and endothelial NO synthase (nNOS and eNOS) to determine correlations with NF-κB activation and inducible NOS (iNOS) expression soon after SCI. Methods. In 48 adult male Wistar rats clip-based (50 g/mm2/10 seconds) SCI was induced, and spinal cords were removed at different intervals for the following evaluations: 1) assaying specific activity of nNOS and eNOS; 2) electrophoresis mobility shift assay for activated NF-κB; 3) Northern blotting for iNOS; 4) immunohistochemistry for iNOS and NF-κB; and 5) immunofluorescence for iNOS and NF-κB. At 15 minutes postinjury, eNOS activity decreased significantly (p < 0.001), as did nNOS activity at 1 hour compared with these levels in control animals and rats killed at 15 and 30 minutes after SCI (...
Because of toxicity at high concentrations, nitric oxide (NO) contributes to spinal cord injury (SCI) secondary lesions. At low concentrations NO modulates nuclear factor–kB (NF-kB) activation. The authors investigated the activity of neuronal and endothelial NO synthase (nNOS and eNOS) to determine correlations with NF- kB activation and inducible NOS (iNOS) expression soon after SCI.
Early nuclear factor-kappaB activation and inducible nitric oxide synthase expression in injured spinal cord neurons correlating with a diffuse reduction of constitutive nitric oxide synthase activity
MISCUSI, MASSIMO;
2006
Abstract
Object. Because of toxicity at high concentrations, nitric oxide (NO) contributes to spinal cord injury (SCI) secondary lesions. At low concentrations NO modulates nuclear factor-κB (NF-κB) activation. The authors investigated the activity of neuronal and endothelial NO synthase (nNOS and eNOS) to determine correlations with NF-κB activation and inducible NOS (iNOS) expression soon after SCI. Methods. In 48 adult male Wistar rats clip-based (50 g/mm2/10 seconds) SCI was induced, and spinal cords were removed at different intervals for the following evaluations: 1) assaying specific activity of nNOS and eNOS; 2) electrophoresis mobility shift assay for activated NF-κB; 3) Northern blotting for iNOS; 4) immunohistochemistry for iNOS and NF-κB; and 5) immunofluorescence for iNOS and NF-κB. At 15 minutes postinjury, eNOS activity decreased significantly (p < 0.001), as did nNOS activity at 1 hour compared with these levels in control animals and rats killed at 15 and 30 minutes after SCI (...I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
