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首页> 外文期刊>Journal of Neurochemistry: Offical Journal of the International Society for Neurochemistry >Ischemic post-conditioning protects brain and reduces inflammation in a rat model of focal cerebral ischemia/reperfusion.
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Ischemic post-conditioning protects brain and reduces inflammation in a rat model of focal cerebral ischemia/reperfusion.

机译:缺血后处理可保护大脑并减少局灶性脑缺血/再灌注大鼠模型的炎症。

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摘要

Ischemic post-conditioning (Post-cond) is a phenomenon in which intermittent interruptions of blood flow in the early phase of reperfusion can protect organ from ischemia/reperfusion (I/R) injury. Recent studies demonstrated ischemic Post-cond reduced infarct size in cerebral I/R injury. However, the molecular mechanisms underlying this phenomenon are not completely understood. As inflammation is known to be detrimental to the neurological outcome during the acute phase after stroke, we investigated whether ischemic Post-cond played its protective role in preventing post-ischemic inflammation in the rat middle cerebral artery occlusion model. Rats were treated with ischemic Post-cond after 60 min of occlusion (beginning of reperfusion). The infarct volume and myeloperoxidase activity were assessed at 24 h. The lipid peroxidation levels was evaluated by malondialdehyde assay and the expressions of interleukin-1beta, tumor necrosis factor-alpha, and intercellular adhesion molecule 1 were studied by RT-PCR or western blotting. Ischemic Post-cond decreased myeloperoxidase activity and expressions of interleukin-1beta, tumor necrosis factor-alpha, and intercellular adhesion molecule 1. Ischemic Post-cond also reduced infarct volume and lipid peroxidation levels. These findings indicated that ischemic Post-cond may be a promising neuroprotective approach for focal cerebral I/R injury and it is achieved, at least in part, by the inhibition of inflammation.
机译:缺血后处理(Post-cond)是一种现象,其中在再灌注的早期间歇性地中断血流可以保护器官免受缺血/再灌注(I / R)的伤害。最近的研究表明,缺血后病情减轻了脑I / R损伤的梗塞面积。但是,这种现象的分子机制尚不完全清楚。由于已知炎症对中风后急性期的神经系统结局有害,因此我们研究了缺血性后cond在大鼠中脑动脉闭塞模型中是否发挥了预防缺血性后炎症的保护作用。闭塞60分钟(再灌注开始)后,对大鼠进行缺血后缺血治疗。在24小时时评估梗塞体积和髓过氧化物酶活性。通过丙二醛分析评估脂质过氧化水平,并通过RT-PCR或蛋白质印迹研究白细胞介素-1β,肿瘤坏死因子-α和细胞间粘附分子1的表达。缺血后抑制骨髓过氧化物酶活性以及白介素-1β,肿瘤坏死因子-α和细胞间粘附分子1的表达。缺血后抑制作用还减少了梗塞体积和脂质过氧化水平。这些发现表明,缺血后治疗可能是局灶性脑I / R损伤的一种有前途的神经保护方法,至少可以通过抑制炎症来实现。

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