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间歇性低压低氧预处理对大鼠脑缺血/再灌注的神经保护作用

Neuroprotective effect of intermittent hypobaric hypoxia preconditioning on cerebral ischemia/reperfusion in rats.

作者信息

Yue Wu, Cunlin Gu, Lu Huang, Yuanqing Zhao, Yanjun Tang, Qiong Wu

机构信息

Department of Pathology, Medical College of Qinghai University Xining 810000, Qinghai, P. R. China.

Department of Biochemistry, Qinghai University Xining 810000, Qinghai, P. R. China.

出版信息

Int J Clin Exp Pathol. 2020 Nov 1;13(11):2860-2869. eCollection 2020.

PMID:33284899
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7716138/
Abstract

BACKGROUND

Ischemic tolerance is an endogenous protective mechanism in organs or tissues undergoing one or more short-term sublethal ischemias. Intermittent hypobaric hypoxia preconditioning (IHHP) can induce tolerance and thus protect brain tissues from cerebral ischemic injury (CIR). The current study evaluated the neuroprotective effect of IHHP.

METHODS

The established xenograft model was divided into the ischemia/reperfusion (I/R), IHHP, IHHP+I/R, and sham groups. Transmission electron microscopy was used to observe alterations in neuron ultrastructure. Neuron damage was detected using Nissl staining. Western blot and qRT-PCR were used to evaluate the relative expression of genes and proteins related to apoptosis. Immunohistochemistry was used to determine the expression of proteins involved in the processes of neuroprotection and repair.

RESULTS

Our results indicated that the damage to the neurons, organelles, and axons was significantly less following ischemia/reperfusion and intermittent hypobaric hypoxia reconditioning treatment than that in the ischemia/reperfusion group. Compared to the ischemia/reperfusion group, significant downregulation of pro-apoptotic gene/protein expressions along with upregulation of anti-apoptotic and nerve regeneration gene/protein expressions in the IHHP+I/R group were observed.

CONCLUSION

IHHP can significantly reduce ischemia/reperfusion injury in rat brain nerves and promote nerve repair.

摘要

背景

缺血耐受是器官或组织经历一次或多次短期亚致死性缺血时的一种内源性保护机制。间歇性低压缺氧预处理(IHHP)可诱导耐受性,从而保护脑组织免受脑缺血损伤(CIR)。本研究评估了IHHP的神经保护作用。

方法

将建立的异种移植模型分为缺血/再灌注(I/R)组、IHHP组、IHHP+I/R组和假手术组。采用透射电子显微镜观察神经元超微结构的变化。使用尼氏染色检测神经元损伤。采用蛋白质免疫印迹法和qRT-PCR评估与凋亡相关的基因和蛋白质的相对表达。采用免疫组织化学法测定参与神经保护和修复过程的蛋白质表达。

结果

我们的结果表明,与缺血/再灌注组相比,缺血/再灌注和间歇性低压缺氧预处理后神经元、细胞器和轴突的损伤明显减轻。与缺血/再灌注组相比,在IHHP+I/R组中观察到促凋亡基因/蛋白表达显著下调,同时抗凋亡和神经再生基因/蛋白表达上调。

结论

IHHP可显著减轻大鼠脑神经的缺血/再灌注损伤并促进神经修复。

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