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首页> 外文期刊>Neurosurgery >Differential cerebral protein synthesis and heat shock protein 70 expression in the core and penumbra of rat brain after transient focal ischemia.
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Differential cerebral protein synthesis and heat shock protein 70 expression in the core and penumbra of rat brain after transient focal ischemia.

机译:短暂性局灶性局部缺血后大鼠大脑核心和半影区差异性脑蛋白合成和热休克蛋白70表达。

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摘要

OBJECTIVE: The purpose of this study was to correlate the cerebral protein synthesis (CPS) reductions in the ischemic core and penumbra with the metabolic stress response indicated by heat shock protein 70 (HSP70) synthesis. METHODS: Rats were subjected to 90 minutes of temporary focal cerebral ischemia produced by occlusion of the middle cerebral artery, using the endovascular suture model. Regional CPS was qualitatively evaluated, with [(35)S]methionine autoradiography, after reperfusion for 2 to 72 hours. The observed changes were correlated with HSP70 immunoreactivity, as assessed in the same brain sections. The ischemic core in the striatum was characterized by HSP70 expression only in endothelial and/or glial cells, with an absence of expression in neurons. The penumbra was delineated as the cortical middle cerebral artery territory region in which HSP70 was also expressed in metabolically stressed neurons. RESULTS: After 2 hours of reperfusion, CPS was reduced to 30 +/- 16% of the homologous contralateral hemisphere value in the core and to 75 +/- 22% in the penumbra (P < 0.05). This difference was still present at 72 hours, when CPS values were 62 +/- 21% and 98 +/- 29% of the nonischemic contralateral hemisphere values in the core and penumbra, respectively (P < 0.05). CONCLUSION: Persistent inhibition of CPS in regions in which neuronal HSP70 expression is absent may distinguish core areas of infarction from penumbral regions in which neuronal HSP70 is present, which eventually recover from sublethal metabolic stress during reperfusion after temporary focal ischemia.
机译:目的:本研究的目的是将缺血性核心和半影的脑蛋白合成(CPS)减少与热休克蛋白70(HSP70)合成所表明的代谢应激反应相关联。方法:使用血管内缝合模型对大鼠进行90分钟的临时性局灶性脑缺血,该缺血是由大脑中动脉闭塞产生的。再灌注2至72小时后,用[(35)S]蛋氨酸放射自显影定性评估区域CPS。如在同一大脑切片中所评估,观察到的变化与HSP70免疫反应性相关。纹状体中的缺血核心的特征是HSP70仅在内皮和/或神经胶质细胞中表达,而在神经元中则没有表达。半影被描绘为皮质中脑动脉区域区域,其中在代谢应激神经元中也表达了HSP70。结果:再灌注2小时后,CPS降低至核心同侧对侧半球值的30 +/- 16%,半影降低至75 +/- 22%(P <0.05)。当CPS值分别为核心和半影区非缺血性对侧半球值的62 +/- 21%和98 +/- 29%时,这种差异在72小时时仍然存在(P <0.05)。结论:在神经元HSP70表达缺失的区域持续抑制CPS可能将梗塞的核心区域与存在神经元HSP70的半影区区分开,最终在暂时性局灶性缺血后的再灌注过程中从亚致死代谢压力中恢复过来。

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