Ischaemic Postconditioning Rescues Brain Injury Caused by Focal Ischaemia/Reperfusion via Attenuation of Protein Oxidization

Ischaemic Postconditioning Rescues Brain Injury Caused by Focal Ischaemia/Reperfusion via Attenuation of Protein Oxidization
复制标题

缺血后处理通过减弱蛋白质氧化来挽救局灶性缺血/再灌注引起的脑损伤

DOI:
10.1177/147323001204000314
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发表时间:
2012-05-01
影响因子:
1.6
通讯作者:
Ge, P. F.
Ge, P. F.
中科院分区:
医学4区
文献类型:
--
作者:
Li, Z. Y.;Liu, B.;Ge, P. F.

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目的:探讨缺血后适应对局灶性缺血再灌注脑损伤及蛋白氧化的影响。方法:30只成年雄性Wistar大鼠随机分为假手术组、缺血组和缺血后适应组。脑中动脉闭塞致缺血,缺血2 h后采用30-s/30-s再灌注/再闭塞3个周期进行缺血后处理。评估脑梗死面积、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,缺血后适应脑梗死的大小明显减小,并伴有蛋白羰基衍生物和AOPPs的显著降低。与缺血组相比,缺血后适应使SOD、CAT和蛋白酶体活性升高。结论:缺血后处理是减少局灶性缺血/再灌注引起的脑梗死的大小和影响的有效方法,可能是由于氧化蛋白水平的降低。因此,减少蛋白质氧化可能是预防脑损伤的有用靶点。
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.