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

• Published in: Archives of medical research Vol. 44; no. 4; pp. 251 - 258
• Main Authors: Dehghan, Fatemeh, Khaksari Hadad, Mohammad, Asadikram, Gholamreza, Najafipour, Hamid, Shahrokhi, Nader
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.05.2013
• Subjects: Animals; Blood-Brain Barrier - drug effects; Blood-Brain Barrier - metabolism; Brain - drug effects; Brain - metabolism; Brain - physiopathology; Brain edema; Brain Edema - drug therapy; Brain Edema - etiology; Brain Edema - metabolism; Brain Edema - physiopathology; Brain Injuries - complications; Brain Injuries - drug therapy; Brain Injuries - metabolism; Brain Injuries - physiopathology; Internal Medicine; Intracranial pressure; Intracranial Pressure - drug effects; Male; Malondialdehyde - metabolism; Melatonin; Melatonin - pharmacology; Melatonin - therapeutic use; Neurological outcomes; Oxidative Stress; Rats; Superoxide Dismutase - metabolism; Melatonin; Brain edema; Neurological outcomes; Intracranial pressure
• DOI: 10.1016/j.arcmed.2013.04.002
• ISSN: 0188-4409

Background and Aims Traumatic 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. Methods Albino 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. Results Brain 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). Conclusion Melatonin decreases brain edema, BBB permeability and ICP, but increases VCS after TBI. These effects are probably due to inhibition of oxidative stress.