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首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >Role of P2X7 purinoceptors in neuroprotective mechanism of ischemic postconditioning in mice
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Role of P2X7 purinoceptors in neuroprotective mechanism of ischemic postconditioning in mice

机译:P2X7嘌呤受体在小鼠缺血后适应神经保护机制中的作用

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Cerebral ischemia-reperfusion (I-R) injury is one of the primary causes of ischemic stroke. Ischemic postconditioning (iPoCo) is evolving as an important adaptive technique to contain I-R injury. Some recent studies have shown neuroprotective effect of iPoCo. However, neuroprotective mechanism of iPoCo is not clear. So, the present study has been undertaken to investigate the possible role of P2X7 purinoceptors in neuroprotective mechanism of iPoCo in mice. Bilateral carotid artery occlusion for 12 min followed by R for 24 h produced a significant rise in cerebral infarct size and neurological severity score (NSS) along with impairment of memory and motor coordination. iPoCo, involving three episodes of 10-s carotid artery occlusion with intermittent R of 10 s applied just after ischemic insult of 12 min, produced a significant decrease in cerebral infarct size and NSS along with reversal of I-R-induced impairment of memory and motor coordination. iPoCo induced neuroprotective effects were significantly abolished by pretreatment with selective purinergic P2X7 receptor blocker Brilliant Blue G (40 mg/kg intraperitoneal). It may be concluded that neuroprotective effect of iPoCo probably involves in activation of purinergic P2X7 receptors.
机译:脑缺血再灌注(I-R)损伤是缺血性中风的主要原因之一。缺血后处理(iPoCo)正在发展成为控制I-R损伤的重要自适应技术。最近的一些研究表明iPoCo的神经保护作用。但是,iPoCo的神经保护机制尚不清楚。因此,进行了本研究以研究P2X7嘌呤受体在iPoCo小鼠神经保护机制中的可能作用。双边颈动脉阻塞12分钟,然后R持续24 h会导致脑梗死面积和神经系统严重程度评分(NSS)显着增加,以及记忆和运动协调障碍。 iPoCo涉及缺血发作12分钟后立即施行的3次10s颈动脉阻塞发作,间歇性R为10 s,导致脑梗死面积和NSS显着减少,以及IR引起的记忆力和运动协调障碍逆转。 iPoCo诱导的神经保护作用被选择性嘌呤能P2X7受体阻滞剂Brilliant Blue G(40 mg / kg腹膜内)预处理所消除。可以得出结论,iPoCo的神经保护作用可能与嘌呤能P2X7受体的激活有关。

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