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缺血后处理通过下调水通道蛋白-4减轻大鼠局灶性脑缺血再灌注后的脑水肿。

Ischemic Postconditioning Alleviates Brain Edema After Focal Cerebral Ischemia Reperfusion in Rats Through Down-Regulation of Aquaporin-4.

作者信息

Han Dong, Sun Miao, He Ping-Ping, Wen Lu-Lu, Zhang Hong, Feng Juan

机构信息

Department of Neurology, Affiliated Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, Liaoning, 110004, People's Republic of China.

出版信息

J Mol Neurosci. 2015 Jul;56(3):722-9. doi: 10.1007/s12031-015-0504-y. Epub 2015 Feb 8.

DOI:10.1007/s12031-015-0504-y
PMID:25662982
Abstract

Cerebral edema is a serious complication associated with cerebral ischemia/reperfusion (I/R). Aquaporin-4 (AQP4) plays a role in generating postischemic edema after reperfusion. Recently, ischemic postconditioning (Postcond) has been shown to produce neuroprotective effects and reduce brain edema in rats after cerebral I/R. It is unclear if ischemic Postcond alleviates brain edema injury through regulation of AQP4. In this study, middle cerebral artery occlusion (MCAO) was induced in rats by filament insertion for 2 h following 24-h reperfusion: ischemic Postcond treatment was performed before reperfusion in the experimental group. We used the wet-dry weight ratio and transmission electron microscopy to evaluate brain edema after 24 h of reperfusion. We used immunohistochemistry and Western blot analyses to evaluate the distribution and expression of AQP4. Ischemic Postcond significantly reduced the water content of the brain tissue and swelling of the astrocytic foot processes. AQP4 expression increased in the I/R and Postcond groups compared to the sham group, but it decreased in the Postcond group compared to the I/R group. The results of our study suggest that ischemic Postcond effectively reduces brain edema after reperfusion by inhibiting AQP4 expression. The data in this study support the use of ischemic Postcond for alleviating brain edema after cerebral I/R.

摘要

脑水肿是与脑缺血/再灌注(I/R)相关的一种严重并发症。水通道蛋白4(AQP4)在再灌注后缺血性水肿的形成中起作用。最近,缺血后适应(Postcond)已被证明可产生神经保护作用,并减轻大鼠脑I/R后的脑水肿。目前尚不清楚缺血后适应是否通过调节AQP4来减轻脑水肿损伤。在本研究中,通过插入线栓诱导大鼠大脑中动脉闭塞(MCAO)2小时,再灌注24小时:实验组在再灌注前进行缺血后适应治疗。我们使用干湿重比和透射电子显微镜评估再灌注24小时后的脑水肿情况。我们使用免疫组织化学和蛋白质印迹分析来评估AQP4的分布和表达。缺血后适应显著降低了脑组织的含水量和星形胶质细胞足突的肿胀。与假手术组相比,I/R组和后适应组中AQP4表达增加,但与I/R组相比,后适应组中AQP4表达降低。我们的研究结果表明,缺血后适应通过抑制AQP4表达有效减轻再灌注后的脑水肿。本研究中的数据支持使用缺血后适应来减轻脑I/R后的脑水肿。

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Melatonin renders neuroprotection by protein kinase C mediated aquaporin-4 inhibition in animal model of focal cerebral ischemia.褪黑素通过蛋白激酶 C 介导的水通道蛋白-4 抑制在局灶性脑缺血动物模型中发挥神经保护作用。
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Ischemic postconditioning protects the neurovascular unit after focal cerebral ischemia/reperfusion injury.
黄芪甲苷对大鼠脑缺血再灌注后高血压的作用。
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No Differences in Cerebral Immunohistochemical Markers following Remote Ischemic Postconditioning in Newborn Piglets with Hypoxia-Ischemia.新生缺氧缺血仔猪远程缺血后处理对脑免疫组织化学标志物无影响。
Neuropediatrics. 2022 Dec;53(6):423-431. doi: 10.1055/a-1889-8544. Epub 2022 Jul 1.
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Perioperative stroke: A perspective on challenges and opportunities for experimental treatment and diagnostic strategies.围手术期卒中:对实验性治疗和诊断策略的挑战和机遇的看法。
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Ischemic postconditioning for stroke treatment: current experimental advances and future directions.用于中风治疗的缺血后适应:当前的实验进展与未来方向
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Advances in intervention methods and brain protection mechanisms of in situ and remote ischemic postconditioning.原位和远程缺血后处理的干预方法和脑保护机制的研究进展。
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