Oxidative stress induced by
spinal cord injury (SCI) has deleterious effects on the function of several organ systems including the urinary bladder. In this study, we investigated the possible protective actions of
melatonin on SCI-induced oxidative damage and urinary bladder dysfunction. Wistar albino rats (n = 24) were divided randomly as control, vehicle- or
melatonin (10 mg/kg, ip)-treated SCI groups. To induce SCI, a standard weight-drop method that induced a moderately severe injury at T10 was used. Injured animals were given either vehicle or
melatonin 15 min postinjury. One week postinjury, each rat was neurologically examined and then decapitated; blood samples were taken to evaluate
neuron-specific enolase (NSE) and soluble
protein 100β (S-100β). Spinal cord (SC) and urinary bladder samples were taken for functional studies and histological examination or stored for the measurement of
malondialdehyde (MDA),
glutathione (GSH) and
nerve growth factor (
NGF) levels and
caspase-3 activity. Isometric contractions in bladder strips were induced by
carbachol. In the SCI rats, decreased contractile responses of the bladder strips were found to be restored by
melatonin treatment. Serum S-100β levels and NSE activities and tissue MDA levels and
caspase-3 activities, all of which were elevated in the vehicle-treated SCI animals as compared to the control values, were reversed by
melatonin treatment. On the other hand, reduced GSH and
NGF levels due to SCI were restored by
melatonin treatment. Furthermore,
melatonin treatment improved histological findings. These findings suggest that
melatonin reduces SCI-induced tissue injury and improves bladder functions through its effects on oxidative stress and
NGF.