Cysteamine Alleviates Early Brain Injury Via Reducing Oxidative Stress and Apoptosis in a Rat Experimental Subarachnoid Hemorrhage Model
Cysteamine Alleviates Early Brain Injury Via Reducing Oxidative Stress and Apoptosis in a Rat Experimental Subarachnoid Hemorrhage Model
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半胱胺通过减少大鼠实验性蛛网膜下腔出血模型中的氧化应激和细胞凋亡来减轻早期脑损伤
DOI：
10.1007/s10571-014-0150-x
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发表时间：
2015-05-01
影响因子：
4
通讯作者：
Sun, Bao-liang
中科院分区：
文献类型：
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作者：
Zhang, Zong-yong;Yang, Ming-feng;Sun, Bao-liang
氧化应激在蛛网膜下腔出血(SAH)后早期脑损伤(EBI)的发病机制中起重要作用。本研究的目的是评估半胱胺是否通过其抗氧化和抗凋亡作用来预防SAH后的氧化应激损伤。结果表明，腹腔注射半胱胺(20 mg/kg/d)可显著减轻SAH大鼠的EBI(包括神经行为缺陷、脑水肿、血脑屏障通透性和皮质神经元凋亡)。同时，半胱胺治疗可降低SAH后48h脑组织中的氧自由基水平，升高脑组织中丙二醛、3-硝基酪氨酸和8-羟基脱氧鸟苷的浓度，增加谷胱甘肽过氧化物酶活性、谷胱甘肽和脑源性神经营养因子的浓度。这些结果表明，半胱胺可以改善SAH模型大鼠的EBI，并对其起到神经保护作用。
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.