TY - GEN
T1 - The antioxidant effects of melatonin after intracerebral hemorrhage in rats
AU - Rojas, H.
AU - Lekic, T.
AU - Chen, W.
AU - Jadhav, V.
AU - Titova, E.
AU - Martin, R. D.
AU - Tang, J.
AU - Zhang, J.
N1 - Part of the Acta Neurochirurgica Supplementum book series (NEUROCHIRURGICA, volume 105) Free radical mechanisms are involved in secondary brain injury after intracerebral hemorrhage (ICH). Since melatonin is a potent free radical scavenger and indirect antioxidant, the objective of this study was to evaluate whether melatonin administration would attenuate oxidative stress, brain edema, and neurological deficits in a rat model of ICH.
PY - 2008/11/12
Y1 - 2008/11/12
N2 - Free radical mechanisms are involved in secondary brain injury after intracerebral hemorrhage (ICH). Since melatonin is a potent free radical scavenger and indirect antioxidant, the objective of this study was to evaluate whether melatonin administration would attenuate oxidative stress, brain edema, and neurological deficits in a rat model of ICH. Animals were assigned into groups consisting of sham (needle trauma), vehicle, and melatonin (15 or 150mg=kg). All injections occurred through the intraperitoneal route, at either 15 min or 3 h after collagenase ICH induction. Then, lipid peroxidation, neurological scoring (18-point system), and brain water content were evaluated at 24 h post-ICH. Results demonstrated dramatically increased lipid peroxidation after collagenase-induced ICH; however, melatonin treatment effectively attenuated this lipid peroxidation. Nonetheless, neurological scoring and brain water content in the right basal ganglia was without significant difference between any treatment regimens (15 or 150mg=kg of melatonin) or time points of drug administration (15 min or 3 h post-ICH). Therefore, melatonin reduced oxidative stress but did not change extent of brain edema or neurologic deficits. © 2008 Springer-Verlag.
AB - Free radical mechanisms are involved in secondary brain injury after intracerebral hemorrhage (ICH). Since melatonin is a potent free radical scavenger and indirect antioxidant, the objective of this study was to evaluate whether melatonin administration would attenuate oxidative stress, brain edema, and neurological deficits in a rat model of ICH. Animals were assigned into groups consisting of sham (needle trauma), vehicle, and melatonin (15 or 150mg=kg). All injections occurred through the intraperitoneal route, at either 15 min or 3 h after collagenase ICH induction. Then, lipid peroxidation, neurological scoring (18-point system), and brain water content were evaluated at 24 h post-ICH. Results demonstrated dramatically increased lipid peroxidation after collagenase-induced ICH; however, melatonin treatment effectively attenuated this lipid peroxidation. Nonetheless, neurological scoring and brain water content in the right basal ganglia was without significant difference between any treatment regimens (15 or 150mg=kg of melatonin) or time points of drug administration (15 min or 3 h post-ICH). Therefore, melatonin reduced oxidative stress but did not change extent of brain edema or neurologic deficits. © 2008 Springer-Verlag.
KW - Melatonin
KW - collagenase
KW - intracerebral hemorrhage
KW - rats
KW - Melatonin/therapeutic use
KW - Antioxidants/therapeutic use
KW - Basal Ganglia/drug effects
KW - Cerebral Hemorrhage/chemically induced
KW - Rats
KW - Male
KW - Rats, Sprague-Dawley
KW - Collagenases
KW - Dose-Response Relationship, Drug
KW - Brain Edema/etiology
KW - Lipid Peroxidation/drug effects
KW - Animals
KW - Neurologic Examination
KW - Time Factors
KW - Disease Models, Animal
UR - https://link.springer.com/content/pdf/10.1007%2F978-3-211-09469-3_4.pdf
UR - https://www.mendeley.com/catalogue/c843888a-c354-3b5b-8edf-118ad2a213de/
U2 - 10.1007/978-3-211-09469-3_4
DO - 10.1007/978-3-211-09469-3_4
M3 - Conference contribution
C2 - 19066075
SN - 9783211094686
SN - 978-3-211-99870-0
T3 - Acta Neurochirurgica, Supplementum
SP - 19
EP - 21
BT - Cerebral Hemorrhage
PB - Springer Vienna
ER -