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海洋化合物卡图纳瑞因在体内和体外通过调节Akt和eNOS的磷酸化来抑制血管生成。

Marine compound catunaregin inhibits angiogenesis through the modulation of phosphorylation of akt and eNOS in vivo and in vitro.

作者信息

Liu Jun-Xiu, Luo Min-Qi, Xia Meng, Wu Qi, Long Si-Mei, Hu Yaohua, Gao Guang-Chun, Yao Xiao-Li, He Mian, Su Huanxing, Luo Xiong-Ming, Yao Shu-Zhong

机构信息

Department of Obstetrics and Gynecology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China.

Department of Clinical Laboratory, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510630, China.

出版信息

Mar Drugs. 2014 May 12;12(5):2790-801. doi: 10.3390/md12052790.

DOI:10.3390/md12052790
PMID:24824025
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4052316/
Abstract

Angiogenesis is the formation of blood vessels from pre-existing vasculature. Excessive or uncontrolled angiogenesis is a major contributor to many pathological conditions whereas inhibition of aberrant angiogenesis is beneficial to patients with pathological angiogenesis. Catunaregin is a core of novel marine compound isolated from mangrove associate. The potential anti-angiogenesis of catunaregin was investigated in human umbilical vein endothelial cells (HUVECs) and zebrafish. HUVECs were treated with different concentrations of catunaregin in the presence or absence of VEGF. The angiogenic phenotypes including cell invasion cell migration and tube formation were evaluated following catunaregin treatment in HUVECs. The possible involvement of AKT, eNOS and ERK1/2 in catunaregin-induced anti-angiogenesis was explored using Western blotting. The anti-angiogenesis of catunaregin was further tested in the zebrafish embryo neovascularization and caudal fin regeneration assays. We found that catunaregin dose-dependently inhibited angiogenesis in both HUVECs and zebrafish embryo neovascularization and zebrafish caudal fin regeneration assays. In addition, catunaregin significantly decreased the phosphorylation of Akt and eNOS, but not the phosphorylation of ERK1/2. The present work demonstrates that catunaregin exerts the anti-angiogenic activity at least in part through the regulation of the Akt and eNOS signaling pathways.

摘要

血管生成是指从已有的脉管系统形成血管。过度或不受控制的血管生成是许多病理状况的主要促成因素，而抑制异常血管生成对患有病理性血管生成的患者有益。卡图纳瑞因是从红树林伴生生物中分离出的一种新型海洋化合物的核心成分。在人脐静脉内皮细胞（HUVECs）和斑马鱼中研究了卡图纳瑞因潜在的抗血管生成作用。在有或没有血管内皮生长因子（VEGF）的情况下，用不同浓度的卡图纳瑞因处理HUVECs。在卡图纳瑞因处理HUVECs后，评估包括细胞侵袭、细胞迁移和管形成在内的血管生成表型。使用蛋白质印迹法探究了Akt、内皮型一氧化氮合酶（eNOS）和细胞外信号调节激酶1/2（ERK1/2）在卡图纳瑞因诱导的抗血管生成中的可能作用。在斑马鱼胚胎血管新生和尾鳍再生试验中进一步测试了卡图纳瑞因的抗血管生成作用。我们发现，在HUVECs、斑马鱼胚胎血管新生和斑马鱼尾鳍再生试验中，卡图纳瑞因均呈剂量依赖性地抑制血管生成。此外，卡图纳瑞因显著降低了Akt和eNOS的磷酸化水平，但未降低ERK1/2的磷酸化水平。目前的研究表明，卡图纳瑞因至少部分地通过调节Akt和eNOS信号通路发挥抗血管生成活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfd/4052316/c182eb075b3e/marinedrugs-12-02790-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfd/4052316/131de85950b8/marinedrugs-12-02790-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfd/4052316/6aa3ca5f6c7f/marinedrugs-12-02790-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfd/4052316/f11a8aa9ed12/marinedrugs-12-02790-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfd/4052316/f8039395ff8f/marinedrugs-12-02790-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfd/4052316/b6759a619967/marinedrugs-12-02790-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfd/4052316/c182eb075b3e/marinedrugs-12-02790-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfd/4052316/131de85950b8/marinedrugs-12-02790-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfd/4052316/6aa3ca5f6c7f/marinedrugs-12-02790-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfd/4052316/f11a8aa9ed12/marinedrugs-12-02790-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfd/4052316/f8039395ff8f/marinedrugs-12-02790-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfd/4052316/b6759a619967/marinedrugs-12-02790-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dfd/4052316/c182eb075b3e/marinedrugs-12-02790-g005.jpg

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