Abstract
Carnosine (β-alanyl-L-histidine) has been demonstrated to provide antioxidative and anti-apoptotic roles in the animal of ischemic brain injuries and neurodegenerative diseases. The aim of this study was to examine whether carnosine prevents subarachnoid hemorrhage (SAH)-induced early brain injury (EBI) in rats. We found that intraperitoneal administration of carnosine improved neurobehavioral deficits, attenuated brain edema and blood-brain barrier permeability, and decreased reactive oxygen species level at 48 h following SAH in rat models. Carnosine treatment increased tissue copper/zinc superoxide dismutase (CuZn-SOD) and glutathione peroxidase (GSH-Px) enzymatic activities, and reduced post-SAH elevated lactate dehydrogenase (LDH) activity, the concentration of malondialdehyde (MDA), 3-nitrotyrosine (3-NT), 8-hydroxydeoxyguanosine (8-OHDG), interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) in rats. Furthermore, carnosine treatment attenuated SAH-induced microglia activation and cortical neuron apoptosis. These results indicated that administration of carnosine may provide neuroprotection in EBI following SAH in rat models.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antigens, Nuclear / metabolism
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Antioxidants / pharmacology
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Antioxidants / therapeutic use*
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Apoptosis* / drug effects
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Behavior, Animal
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Blood-Brain Barrier / drug effects
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Blood-Brain Barrier / pathology
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Brain Edema / complications
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Brain Edema / drug therapy
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Brain Edema / pathology
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Brain Injuries / complications
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Brain Injuries / drug therapy*
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Brain Injuries / pathology
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Carnosine / pharmacology
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Carnosine / therapeutic use*
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Caspase 3 / metabolism
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Cerebral Cortex / drug effects
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Cerebral Cortex / pathology
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Cytokines / metabolism
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DNA / metabolism
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Disease Models, Animal
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Fluorescent Antibody Technique
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Glutathione Peroxidase / metabolism
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In Situ Nick-End Labeling
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Lipids / chemistry
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Male
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Microglia / drug effects
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Microglia / pathology
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Nerve Tissue Proteins / metabolism
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Oxidation-Reduction / drug effects
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Permeability / drug effects
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Rats, Sprague-Dawley
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Reactive Oxygen Species / metabolism
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Subarachnoid Hemorrhage / complications
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Subarachnoid Hemorrhage / drug therapy*
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Subarachnoid Hemorrhage / pathology
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Superoxide Dismutase / metabolism
Substances
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Antigens, Nuclear
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Antioxidants
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Cytokines
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Lipids
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Nerve Tissue Proteins
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Rbfox3 protein, rat
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Reactive Oxygen Species
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Carnosine
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DNA
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Glutathione Peroxidase
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Superoxide Dismutase
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Caspase 3