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缺血后处理通过减轻蛋白质氧化来挽救局灶性缺血/再灌注引起的脑损伤。

Ischaemic postconditioning rescues brain injury caused by focal ischaemia/reperfusion via attenuation of protein oxidization.

作者信息

Li Z Y, Liu B, Yu J, Yang F W, Luo Y N, Ge P F

机构信息

Department of Neurosurgery, First Bethune Hospital of Jilin University, Changchun, China.

出版信息

J Int Med Res. 2012;40(3):954-66. doi: 10.1177/147323001204000314.

DOI:10.1177/147323001204000314
PMID:22906268
Abstract

OBJECTIVE

To investigate the effects of ischaemic postconditioning on brain injury and protein oxidization in focal ischaemia/reperfusion.

METHODS

Adult male Wistar rats (n = 30) were randomly divided into sham-operated, ischaemia, and ischaemic postconditioning groups. Ischaemia was produced by middle cerebral artery occlusion and ischaemic postconditioning was performed using three cycles of 30-s/30-s reperfusion/reocclusion after 2 h of ischaemia. Brain infarction size, hydrogen peroxide concentration, superoxide dismutase (SOD), catalase (CAT) and proteasome activities, protein carbonyl derivatives and advanced oxidized protein products (AOPPs) were evaluated.

RESULTS

The size of brain infarction after ischaemic postconditioning was significantly smaller compared with the ischaemia group, and was concomitant with significant reduction in protein carbonyl derivatives and AOPPs. The activities of SOD, CAT and proteasomes were elevated by ischaemic postconditioning compared with the ischaemia group.

CONCLUSIONS

Ischaemic postconditioning is an effective way of reducing the size and effects of brain infarction caused by focal ischaemia/reperfusion, possibly due to a decrease in oxidized protein levels. Decreasing protein oxidization may, therefore, be a useful target for preventing cerebral injury.

摘要

目的

研究缺血后处理对局灶性缺血/再灌注脑损伤及蛋白质氧化的影响。

方法

将30只成年雄性Wistar大鼠随机分为假手术组、缺血组和缺血后处理组。采用大脑中动脉闭塞法制造缺血模型,缺血2小时后进行缺血后处理,即进行3个周期的30秒再灌注/30秒再闭塞。评估脑梗死体积、过氧化氢浓度、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和蛋白酶体活性、蛋白质羰基衍生物和晚期氧化蛋白产物(AOPPs)。

结果

与缺血组相比,缺血后处理后脑梗死体积明显减小,同时蛋白质羰基衍生物和AOPPs显著减少。与缺血组相比,缺血后处理使SOD、CAT和蛋白酶体的活性升高。

结论

缺血后处理是减轻局灶性缺血/再灌注所致脑梗死体积及影响的有效方法,可能是由于氧化蛋白水平降低。因此,降低蛋白质氧化可能是预防脑损伤的一个有用靶点。

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