Effect of Melatonin on Intracranial Pressure and Brain Edema Following Traumatic Brain Injury: Role of Oxidative Stresses

Background and Aims tic brain injury (TBI) is one of the main causes of brain edema and increased intracranial pressure (ICP). In the clinic it is essential to limit the development of ICP after TBI. In the present study, the effects of melatonin on these parameters at different time points and alterations of oxidant factors as one of the probable involved mechanisms have been evaluated. s N-Mary rats were divided into five groups of sham, TBI, TBI + vehicle, TBI + Mel5 and TBI + Mel20. Brain injury was induced by Marmarou method. Melatonin was injected i.p. at 1, 24, 48 and 72 h after brain trauma. Brain water and Evans blue dye contents as well as oxidant/antioxidant factors were measured 72 h after TBI. ICP and neurological scores were determined at −1, 1, 24, 48 and 72 h post-TBI. s water and Evans blue dye contents in melatonin-treated groups decreased as compared to the TBI + vehicle group (p <0.001). Veterinary coma scale (VCS) at 24, 48 and 72 h after TBI showed a significant increase in melatonin groups (TBI + Mel5: p <0.01and TBI + Mel20: p <0.001) in comparison to the TBI + vehicle group. ICP at 24, 48 and 72 h after TBI decreased in melatonin groups as compared to the TBI + vehicle group (p <0.001). Superoxide dismutase and glutathione peroxidase activities showed a significant increase, whereas malondialdehyde level in these groups was significantly lower in melatonin groups in comparison to the TBI + vehicle group (p <0.001). sion nin decreases brain edema, BBB permeability and ICP, but increases VCS after TBI. These effects are probably due to inhibition of oxidative stress.