title: Cysteamine alleviates early brain injury via reducing oxidative stress and apoptosis in a rat experimental subarachnoid hemorrhage model.
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.
authors.affiliation: Key Lab of Cerebral Microcirculation at the Universities of Shandong, Life Science Research Centre of Taishan Medical University, Taian, 271016, Shandong, China, zongyongzhanghust@gmail.com.
authors.forename: Zong-Yong
authors.initials: ZY
authors.lastname: Zhang
authors.forename: Ming-Feng
authors.initials: MF
authors.lastname: Yang
authors.forename: Tao
authors.initials: T
authors.lastname: Wang
authors.forename: Da-Wei
authors.initials: DW
authors.lastname: Li
authors.forename: Yun-Lin
authors.initials: YL
authors.lastname: Liu
authors.forename: Jin-Hui
authors.initials: JH
authors.lastname: Zhang
authors.forename: Bao-Liang
authors.initials: BL
authors.lastname: Sun
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001522:Behavior, Animal; D001812:Blood-Brain Barrier / Q000187:drug effects / Q000473:pathology; D001929:Brain Edema / Q000150:complications / Q000188:drug therapy / Q000473:pathology; D001930:Brain Injuries / Q000150:complications / Q000188:drug therapy* / Q000473:pathology*; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D053148:Caspase 3 / Q000378:metabolism; D002540:Cerebral Cortex / Q000187:drug effects / Q000473:pathology; D003543:Cysteamine / Q000494:pharmacology / Q000627:therapeutic use*; D004195:Disease Models, Animal; D005455:Fluorescent Antibody Technique; D020287:In Situ Nick-End Labeling; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D010539:Permeability / Q000187:drug effects; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000188:drug therapy* / Q000473:pathology*
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D017382:Reactive Oxygen Species; D003543:Cysteamine; D053148:Caspase 3