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自发性高血压大鼠中通过ERK/NF-κB途径对急性缺血性中风作出反应时血管紧张素转换酶的上调。

Up-regulation of angiotensin-converting enzyme in response to acute ischemic stroke via ERK/NF-κB pathway in spontaneously hypertensive rats.

作者信息

Ou Zhou, Tao Meng-Xing, Gao Qing, Zhang Xue-Ling, Yang Yang, Zhou Jun-Shan, Zhang Ying-Dong

机构信息

Department of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, People's Republic of China.

Department of Neurology, Suqian City People's Hospital, Suqian, People's Republic of China.

出版信息

Oncotarget. 2017 Sep 22;8(57):97041-97051. doi: 10.18632/oncotarget.21156. eCollection 2017 Nov 14.

DOI:10.18632/oncotarget.21156
PMID:29228591
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5722543/
Abstract

Cerebral ischemic stroke is usually caused by a temporary or permanent decrease in blood supply to the brain. Despite general progress in diagnosis and treatment, the prognosis of stroke is still unsatisfactory, and more detailed potential mechanisms are needed to investigate underlying the pathological process. Here, we showed that serum angiotensin-converting enzyme (ACE) concentration was positively correlated with infarct volume after acute ischemic stroke (AIS). Moreover, using a permanent middle cerebral artery occlusion rat model, we indicated for the first time that increased ACE expression in response to AIS was regulated by the ERK/NF-κB pathway in peri-infarct regions. More importantly, we disclosed that angiotensin II type 1 receptors were implicated in up-regulation of ACE expression in peri-infarct regions. These findings offer insight into ACE expression and activity in response to stroke, and further our understanding of ACE mechanisms.

摘要

脑缺血性中风通常是由大脑血液供应的暂时或永久性减少引起的。尽管在诊断和治疗方面取得了总体进展，但中风的预后仍然不尽人意，需要更详细的潜在机制来研究其病理过程的基础。在此，我们表明急性缺血性中风（AIS）后血清血管紧张素转换酶（ACE）浓度与梗死体积呈正相关。此外，使用永久性大脑中动脉闭塞大鼠模型，我们首次表明AIS后梗死周围区域中ACE表达的增加是由ERK/NF-κB途径调节的。更重要的是，我们发现1型血管紧张素II受体与梗死周围区域中ACE表达的上调有关。这些发现为中风后ACE的表达和活性提供了见解，并进一步加深了我们对ACE机制的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2306/5722543/b3bb290d7328/oncotarget-08-97041-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2306/5722543/511948db8cc1/oncotarget-08-97041-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2306/5722543/f5538f2b4c87/oncotarget-08-97041-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2306/5722543/49967a57fdf0/oncotarget-08-97041-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2306/5722543/83c95af9b871/oncotarget-08-97041-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2306/5722543/c3e2d27b7ac1/oncotarget-08-97041-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2306/5722543/b3bb290d7328/oncotarget-08-97041-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2306/5722543/511948db8cc1/oncotarget-08-97041-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2306/5722543/f5538f2b4c87/oncotarget-08-97041-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2306/5722543/49967a57fdf0/oncotarget-08-97041-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2306/5722543/83c95af9b871/oncotarget-08-97041-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2306/5722543/c3e2d27b7ac1/oncotarget-08-97041-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2306/5722543/b3bb290d7328/oncotarget-08-97041-g006.jpg

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