Dec 21, 2014

Cysteamine alleviates early brain injury via reducing oxidative stress and apoptosis in a rat experimental subarachnoid hemorrhage model

Cellular and Molecular Neurobiology
Zong-Yong ZhangBao-Liang Sun

Abstract

Oxidative stress plays an important role in the pathogenesis of early brain injury (EBI) following subarachnoid hemorrhage (SAH). The aim of this study was to assess whether cysteamine prevents post-SAH oxidative stress injury via its antioxidative and anti-apoptotic effects. It was observed that intraperitoneal administration of cysteamine (20 mg/kg/day) could significantly alleviate EBI (including neurobehavioral deficits, brain edema, blood-brain barrier permeability, and cortical neuron apoptosis) after SAH in rats. Meanwhile, cysteamine treatment reduced post-SAH elevated the reactive oxygen species level, the concentration of malondialdehyde, 3-nitrotyrosine, and 8-hydroxydeoxyguanosine and increased the glutathione peroxidase enzymatic activity, the concentration of glutathione and brain-derived neurotrophic factor in brain cortex at 48 h after SAH. These results indicated that administration of cysteamine may ameliorate EBI and provide neuroprotection after SAH in rat models.

Mentioned in this Paper

Brain Injuries
Mild Traumatic Brain Injury
Pathogenic Aspects
Immunofluorescence Assay
Blood - Brain Barrier Anatomy
Behavior, Animal
Neurobehavioral Manifestations
Cortex Bone Disorders
Adrenal Cortex Diseases
Pathogenesis

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