Kori L Brewer1, J Shane Hardin. 1. Department of Emergenvy Medicine, Brody School of Medicine at East Carolina University, Greenville, NC 27858, USA. brewerk@mail.ecu.edu
Abstract
OBJECTIVE: To investigate the ability of nicotinamide to protect against secondary damage in spinal cord tissue after an experimental injury. Trauma to the spinal cord induces a cascade of cellular events that lead to progressive tissue injury over time. Nicotinamide has been shown to affect many elements of this cascade, including excitatory amino acid release, inflammation, apoptosis, and cellular energy balance. METHODS: Male Long-Evans (n = 12) rats received an excitotoxic spinal cord injury by intraspinal injection of quisqualic acid (QUIS), a glutamate receptor agonist. A second set of rats (n = 4) received intraspinal saline as a sham injury. Thirty minutes after injury, animals that had QUIS injections received an intraperitoneal injection of either saline (control, n = 4) or nicotinamide (500 mg/kg, n = 8). Seven days postinjury, the spinal cords were removed, and serial sections were cut, mounted on slides, and stained. By using light microscopy, the extent of tissue damage was assessed at the epicenter of injury as well as sections up to 450- microm rostral and 450- microm caudal to the epicenter. RESULTS: Only those animals receiving QUIS injections showed damaged tissue. There was no significant difference in the amount of damage at the epicenter of injury between the saline- and nicotinamide-treated animals. However, when comparing the total amounts of damage over the 975- microm length of cord examined, the rostro-caudal extent of injury was significantly reduced in the nicotinamide-treated animals compared with the saline-treated animals. CONCLUSIONS: Systemic nicotinamide serves to limit the rostro-caudal extent of cell death after experimental spinal cord injury.
OBJECTIVE: To investigate the ability of nicotinamide to protect against secondary damage in spinal cord tissue after an experimental injury. Trauma to the spinal cord induces a cascade of cellular events that lead to progressive tissue injury over time. Nicotinamide has been shown to affect many elements of this cascade, including excitatory amino acid release, inflammation, apoptosis, and cellular energy balance. METHODS: Male Long-Evans (n = 12) rats received an excitotoxic spinal cord injury by intraspinal injection of quisqualic acid (QUIS), a glutamate receptor agonist. A second set of rats (n = 4) received intraspinal saline as a sham injury. Thirty minutes after injury, animals that had QUIS injections received an intraperitoneal injection of either saline (control, n = 4) or nicotinamide (500 mg/kg, n = 8). Seven days postinjury, the spinal cords were removed, and serial sections were cut, mounted on slides, and stained. By using light microscopy, the extent of tissue damage was assessed at the epicenter of injury as well as sections up to 450- microm rostral and 450- microm caudal to the epicenter. RESULTS: Only those animals receiving QUIS injections showed damaged tissue. There was no significant difference in the amount of damage at the epicenter of injury between the saline- and nicotinamide-treated animals. However, when comparing the total amounts of damage over the 975- microm length of cord examined, the rostro-caudal extent of injury was significantly reduced in the nicotinamide-treated animals compared with the saline-treated animals. CONCLUSIONS: Systemic nicotinamide serves to limit the rostro-caudal extent of cell death after experimental spinal cord injury.
Authors: Wesley A Hendricks; Elena S Pak; J Paul Owensby; Kristie J Menta; Margarita Glazova; Justin Moretto; Sarah Hollis; Kori L Brewer; Alexander K Murashov Journal: Mol Med Date: 2006 Jan-Mar Impact factor: 6.354