Abstract
Primary impact to the spinal cord results in rapid increase in tissue oxidative stress which potentiates the initial trauma. In the present study, we hypothesize that altered expression of nitric oxide synthase may be responsible for these effects. Nicotine can exert potent antioxidant and neuroprotective effects in spinal cord injury (SCI). Therefore, the aim of the present study is to evaluate if administration of nicotine can influence expression of inducible nitric oxide synthase (iNOS) and/or neuronal nitric oxide synthase (nNOS) in injured spinal cords. Adult male Long‐Evans rats were subjected to a moderate contusion model of SCI induced by a 10‐gram weight drop from 12.5 mm onto the T‐10 segment. Rats received a single s.c. injection of either saline or nicotine (0.35, 3.5 or 7 mg/kg) two hours after SCI. Spinal cord trauma increased both iNOS and nNOS mRNA and protein levels in the thoracic and lumbar regions of the spinal cords. Treatment with nicotine significantly and in dose‐dependent manner protected against overexpression of iNOS both in the thoracic and lumbar regions of rats with SCI. In contrast, nicotine administration did not affect nNOS expression in injured rats. The present results suggest that protection against overexpression of iNOS may be one of the critical mechanisms of neuroprotective effects of nicotine in SCI.
Supported by Philip Morris USA Inc. and Philip Morris International.