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缺血后处理可保护大脑并减轻局灶性脑缺血/再灌注大鼠模型中的炎症反应。

Ischemic post-conditioning protects brain and reduces inflammation in a rat model of focal cerebral ischemia/reperfusion.

作者信息

Xing Bianzhi, Chen Hui, Zhang Min, Zhao Dongming, Jiang Rui, Liu Xiuheng, Zhang Suming

机构信息

Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

出版信息

J Neurochem. 2008 Jun;105(5):1737-45. doi: 10.1111/j.1471-4159.2008.05276.x. Epub 2008 Feb 4.

Abstract

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.

摘要

缺血后适应(Post-cond)是一种现象,即在再灌注早期间歇性中断血流可保护器官免受缺血/再灌注(I/R)损伤。最近的研究表明,缺血后适应可减小脑I/R损伤中的梗死灶大小。然而,这一现象背后的分子机制尚未完全明确。由于已知炎症对中风后急性期的神经学转归有害,我们研究了在大鼠大脑中动脉闭塞模型中,缺血后适应是否通过预防缺血后炎症发挥其保护作用。在闭塞60分钟后(再灌注开始)对大鼠进行缺血后适应处理。在24小时时评估梗死体积和髓过氧化物酶活性。通过丙二醛测定评估脂质过氧化水平,并通过逆转录-聚合酶链反应(RT-PCR)或蛋白质印迹法研究白细胞介素-1β、肿瘤坏死因子-α和细胞间黏附分子1的表达。缺血后适应降低了髓过氧化物酶活性以及白细胞介素-1β、肿瘤坏死因子-α和细胞间黏附分子1的表达。缺血后适应还减小了梗死体积并降低了脂质过氧化水平。这些发现表明,缺血后适应可能是一种有前景的局灶性脑I/R损伤神经保护方法,并且至少部分是通过抑制炎症实现的。

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