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解偶联蛋白在人脑缺血性病变中的表达增强。

Amplified expression of uncoupling proteins in human brain ischemic lesions.

作者信息

Nakase Taizen, Yoshida Yasuji, Nagata Ken

机构信息

Department of Neurology, Research Institute for Brain and Blood Vessels, Akita, Japan.

出版信息

Neuropathology. 2007 Oct;27(5):442-7. doi: 10.1111/j.1440-1789.2007.00815.x.

DOI:10.1111/j.1440-1789.2007.00815.x
PMID:18018477
Abstract

Uncoupling proteins (UCPs) are reported to regulate mitochondrial respiration and energy metabolism during hibernation. Recently, it has been reported that UCP2 and UCP5 might reduce free radical stress in the ischemic condition in in vitro models, suggesting both as potential neuroprotective agents. We therefore investigated the levels of UCP2 and UCP5 expression in the lesion of human brain infarction. Brain slice sections were prepared from pathological samples collected at our hospital. Embolic stroke brains sectioned because of the stroke (n = 5) and multiple brain infarction with several stroke episodes (n = 4) were selected for this study. We observed the amount of UCP2 and UCP5 expression in both lesioned and intact areas, and compared them between embolic stroke and multiple infarction cases. The results showed that the expression of UCP2 and UCP5 was significantly elevated in the ischemic lesions compared to the intact area. UCP5 expression in the lesions was higher in multiple infarction cases than in embolic stroke cases. In conclusion, brains may respond to neuroprotection through the increased expression of UCP2 and UCP5 under ischemic conditions. Moreover, UCP5 may respond to repetitive ischemic stresses or have a long-term effect.

摘要

据报道,解偶联蛋白(UCPs)在冬眠期间调节线粒体呼吸和能量代谢。最近,有报道称,在体外模型中,UCP2和UCP5可能会减轻缺血状态下的自由基应激,这表明二者均为潜在的神经保护剂。因此,我们研究了人脑梗死病灶中UCP2和UCP5的表达水平。脑切片取自我院收集的病理样本。本研究选取了因中风而切片的栓塞性中风脑(n = 5)和有多次中风发作的多发性脑梗死(n = 4)。我们观察了UCP2和UCP5在病灶区和完整区域的表达量,并比较了栓塞性中风和多发性梗死病例之间的差异。结果显示,与完整区域相比,缺血病灶中UCP2和UCP5的表达显著升高。多发性梗死病例病灶中的UCP5表达高于栓塞性中风病例。总之,大脑可能在缺血条件下通过增加UCP2和UCP5的表达来对神经保护做出反应。此外,UCP5可能对重复性缺血应激做出反应或具有长期作用。

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