Abstract
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.
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Rojas, H. et al. (2008). The antioxidant effects of melatonin after intracerebral hemorrhage in rats. In: Zhou, LF., et al. Cerebral Hemorrhage. Acta Neurochirurgica Supplementum, vol 105. Springer, Vienna. https://doi.org/10.1007/978-3-211-09469-3_4
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DOI: https://doi.org/10.1007/978-3-211-09469-3_4
Publisher Name: Springer, Vienna
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