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首页> 外文期刊>Life sciences >Melatonin renders neuroprotection by protein kinase C mediated aquaporin-4 inhibition in animal model of focal cerebral ischemia
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Melatonin renders neuroprotection by protein kinase C mediated aquaporin-4 inhibition in animal model of focal cerebral ischemia

机译：褪黑素通过蛋白激酶C介导的aquaporin-4抑制作用在局灶性脑缺血动物模型中提供神经保护作用

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Aim: Aquaporin-4(AQP4) expression in the brain with relation to edema formation following focal cerebral ischemia was investigated. Studies have shown that brain edema is one of the significant factors in worsening stroke outcomes. While many mechanisms may aggravate brain injury, one such potential system may involve AQP4 up regulation in stroke patients that could result in increased edema formation. Post administration of melatonin following ischemic stroke reduces AQP4 mediated brain edema and confers neuroprotection. Materials and methods: An in-silico approach was undertaken to confirm effective melatonin-AQP4 binding. Rats were treated with 5 mg/kg, i.p. melatonin or placebo at 30 min prior, 60 min post and 120 min post 60 min of middle cerebral artery occlusion (MCAO) followed by 24 h reperfusion. Rats were evaluated for battery of neurological and motor function tests just before sacrifice. Brains were harvested for infarct size estimation, water content measurement, biochemical analysis, apoptosis study and western blot experiments. Key findings: Melatonin at 60 min post ischemia rendered neuroprotection as evident by reduction in cerebral infarct volume, improvement in motor and neurological deficit and reduction in brain edema. Furthermore, ischemia induced surge in levels of nitrite and malondialdehyde (MDA) were also found to be significantly reduced in ischemic brain regions in treated animals. Melatonin potentiated intrinsic antioxidant status, inhibited acid mediated rise in intracellular calcium levels, decreased apoptotic cell death and also markedly inhibited protein kinase C (PKC) influenced AQP4 expression in the cerebral cortex and dorsal striatum. Significance: Melatonin confers neuroprotection by protein kinase C mediated AQP4 inhibition in ischemic stroke.
机译：目的：研究局灶性脑缺血后脑中水通道蛋白4（AQP4）的表达与水肿形成的关系。研究表明，脑水肿是导致卒中恶化的重要因素之一。尽管许多机制可能加重脑损伤，但其中一种潜在的系统可能涉及中风患者中AQP4的上调，可能导致水肿形成增加。缺血性中风后褪黑激素的给药减少了AQP4介导的脑水肿并赋予了神经保护作用。材料和方法：采用计算机模拟方法确认褪黑激素与AQP4的有效结合。用5mg / kg，腹膜内注射处理大鼠。褪黑素或安慰剂在大脑中部动脉闭塞（MCAO）的60分钟之前，30分钟之后，60分钟之后和120分钟之后，再进行24小时再灌注。处死前对大鼠进行神经和运动功能测试。收集大脑用于梗塞大小估计，水分含量测量，生化分析，细胞凋亡研究和蛋白质印迹实验。关键发现：缺血后60分钟时褪黑激素可通过减少脑梗死体积，改善运动和神经功能缺损以及减少脑水肿来提供神经保护作用。此外，还发现缺血引起的缺血性脑区域中亚硝酸盐和丙二醛（MDA）水平的激增明显减少。褪黑素增强了固有的抗氧化剂状态，抑制了酸介导的细胞内钙水平的升高，凋亡细胞死亡的减少，并且还显着抑制了蛋白激酶C（PKC）影响了大脑皮层和背侧纹状体中AQP4的表达。意义：褪黑素在缺血性中风中通过蛋白激酶C介导的AQP4抑制作用赋予神经保护作用。

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