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去甲肾上腺素通过蛋白激酶C/核因子κB介导的NADPH氧化酶2上调促进血管外膜成纤维细胞中的氧化应激。

Norepinephrine promotes oxidative stress in vascular adventitial fibroblasts via PKC/NFκB-mediated NOX2 upregulation.

作者信息

Wang Yi-Ming, Dong Hong-Ke, Dai Min, Wang Jing-Xiao, Xu Xiao-Yu, Zhu Guo-Qing, Li Xiu-Zhen

机构信息

Department of Physiology, Nanjing Medical University, Nanjing, People's Republic of China.

Department of Cardiology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.

出版信息

Redox Rep. 2025 Dec;30(1):2494314. doi: 10.1080/13510002.2025.2494314. Epub 2025 Apr 23.

DOI:10.1080/13510002.2025.2494314
PMID:40269356
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12024498/
Abstract

BACKGROUND

Sympathetic overactivity is closely associated with vascular remodeling. Sympathetic fibers dominantly innervate the adventitia of arteries rather than tunica media. Vascular adventitial fibroblasts (VAFs) play crucial roles in vascular remodeling. However, the link between sympathetic overactivity and VAF proliferation and migration is unknown.

METHODS

Primary VAFs were isolated from the thoracic aorta of spontaneously hypertensive rats and Wistar-Kyoto rats. Norepinephrine (NE) bitartrate monohydrate was applied to VAFs to simulate the sympathetic overactivity.

RESULTS

NE increased NADPH oxidase (NOX) 2 expression and superoxide level, which were almost abolished by NOX2 inhibitor GSK2795039 or α-adrenoceptor antagonist prazosin, but not significantly affected by NOX1 inhibitor ML171, NOX4 inhibitor GLX351322 or β-adrenoceptor antagonist propranolol. Superoxide scavenger tempol or NOX2 inhibitor GSK2795039 attenuated NE-induced VAF proliferation and migration. NE promoted protein kinase C (PKC) phosphorylation and NFκB-p65 nuclear translocation. Either PKC inhibitor Go6983 or NFκB inhibitor BAY11-7082 attenuated NE-induced NOX activation, NOX2 upregulation, superoxide production, proliferation and migration.

CONCLUSION

NE promotes oxidative stress by α-receptor/PKC/NFκB-mediated NOX2 upregulation, which contributes to proliferation and migration of VAFs.

摘要

背景

交感神经过度活跃与血管重塑密切相关。交感神经纤维主要支配动脉外膜而非中膜。血管外膜成纤维细胞（VAFs）在血管重塑中起关键作用。然而，交感神经过度活跃与VAFs增殖和迁移之间的联系尚不清楚。

方法

从自发性高血压大鼠和Wistar-Kyoto大鼠的胸主动脉中分离出原代VAFs。将酒石酸去甲肾上腺素一水合物应用于VAFs以模拟交感神经过度活跃。

结果

去甲肾上腺素增加了NADPH氧化酶（NOX）2的表达和超氧化物水平，NOX2抑制剂GSK2795039或α-肾上腺素能受体拮抗剂哌唑嗪几乎完全消除了这些作用，但NOX1抑制剂ML171、NOX4抑制剂GLX351322或β-肾上腺素能受体拮抗剂普萘洛尔对其影响不显著。超氧化物清除剂tempol或NOX2抑制剂GSK2795039减弱了去甲肾上腺素诱导的VAFs增殖和迁移。去甲肾上腺素促进蛋白激酶C（PKC）磷酸化和NFκB-p65核转位。PKC抑制剂Go6983或NFκB抑制剂BAY11-7082均可减弱去甲肾上腺素诱导的NOX激活、NOX2上调、超氧化物生成、增殖和迁移。

结论

去甲肾上腺素通过α受体/PKC/NFκB介导的NOX2上调促进氧化应激，这有助于VAFs的增殖和迁移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd8/12024498/746bd7146a22/YRER_A_2494314_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd8/12024498/702e53bbf439/YRER_A_2494314_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd8/12024498/07c282092a5a/YRER_A_2494314_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd8/12024498/549f009b19a3/YRER_A_2494314_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd8/12024498/67dec498807a/YRER_A_2494314_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd8/12024498/a1f33a2012e4/YRER_A_2494314_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd8/12024498/38f25d9ef02f/YRER_A_2494314_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd8/12024498/746bd7146a22/YRER_A_2494314_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd8/12024498/702e53bbf439/YRER_A_2494314_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd8/12024498/07c282092a5a/YRER_A_2494314_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd8/12024498/549f009b19a3/YRER_A_2494314_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd8/12024498/67dec498807a/YRER_A_2494314_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd8/12024498/a1f33a2012e4/YRER_A_2494314_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd8/12024498/38f25d9ef02f/YRER_A_2494314_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecd8/12024498/746bd7146a22/YRER_A_2494314_F0007_OC.jpg

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