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首页> 外文期刊>CNS neuroscience & therapeutics. >M9, A Novel Region of Amino‐Nogo‐A, Attenuates Cerebral Ischemic Injury by Inhibiting NADPH Oxidase‐Derived Superoxide Production in Mice
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M9, A Novel Region of Amino‐Nogo‐A, Attenuates Cerebral Ischemic Injury by Inhibiting NADPH Oxidase‐Derived Superoxide Production in Mice

机译：M9是一种新型的Amino-Nogo-A区域，通过抑制小鼠NADPH氧化酶衍生的超氧化物生成来减轻脑缺血性损伤。

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Summary Aims In acute stroke, neurological damage is due to oxidative stress and neuronal apoptotic death. This study investigated whether Nogo‐A 290‐562 residues region (M9), fused to the transduction domain of the HIV trans‐activator ( TAT ) protein, is neuroprotective against cerebral ischemia and the mechanisms. Methods Transient focal cerebral ischemia was induced by middle cerebral artery occlusion in male C57 BL /6J mice. TAT ‐M9, its mutation or vehicle was applied via intraperitoneal injection at the onset of reperfusion. The neurobehavioral scores, infarction volumes, neuronal apoptosis, and the ratio of Bax/Bcl‐2 were evaluated. Malondialdehyde ( MDA ), reactive oxygen species ( ROS ) levels, and NADPH oxidase activation were measured in the presence or absence of the NADPH oxidase inhibitor apocynin or activator tetrabromocinnamic acid ( TBCA ). Results Immunofluorescence results confirmed that TAT ‐M9 was transduced into brain parenchyma, and it significantly improved neurological behavior, reduced infarct volumes, protected neuronal cells from apoptosis, inhibited activation of NADPH oxidase, and decreased MDA and ROS contents. Furthermore, apocynin imitated the beneficial effects of TAT ‐M9, while TBCA abolished them. Conclusions Our results demonstrate that TAT ‐M9 administration attenuates cerebral ischemia by inhibiting NADPH oxidase‐mediated oxidative damage and neuronal apoptosis in mice. TAT ‐M9 may be a potential treatment for cerebrovascular disease.
机译：摘要目的在急性中风中，神经系统损伤是由于氧化应激和神经元凋亡死亡所致。这项研究调查了Nogo-A 290-562残基区域（M9）与HIV反式激活因子（TAT）蛋白的转导域融合后是否对脑缺血具有神经保护作用及其机制。方法雄性C57 BL / 6J小鼠大脑中动脉闭塞诱发短暂性局灶性脑缺血。 TAT-M9，其突变或媒介物在再灌注开始时通过腹膜内注射应用。评估了神经行为评分，梗死体积，神经元凋亡和Bax / Bcl-2的比率。在存在或不存在NADPH氧化酶抑制剂Apocynin或活化剂四溴肉桂酸（TBCA）的情况下，测量丙二醛（MDA），活性氧（ROS）水平和NADPH氧化酶活化。结果免疫荧光结果证实，TAT-M9被转导至脑实质，并显着改善神经行为，减少梗塞体积，保护神经元细胞免于凋亡，抑制NADPH氧化酶活化以及降低MDA和ROS含量。此外，载脂蛋白原模仿了TAT-M9的有益作用，而TBCA则废除了它们。结论我们的结果表明，TAT-M9给药可通过抑制NADPH氧化酶介导的氧化损伤和小鼠神经元凋亡来减轻脑缺血。 TAT-M9可能是脑血管疾病的潜在治疗方法。

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