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阿朴穿心莲内酯 A 通过抑制 VEGF 信号通路发挥抗血管生成作用。

Anti-Angiogenic Effect of Asperchalasine A Via Attenuation of VEGF Signaling.

机构信息

Department of Food Science and Biotechnology, Kyonggi University, Suwon 16227, Korea.

Institute of Pharmaceutical Science and Technology and College of Pharmacy, Hanyang University, Ansan 15588, Korea.

出版信息

Biomolecules. 2019 Aug 12;9(8):358. doi: 10.3390/biom9080358.

DOI:10.3390/biom9080358
PMID:31408989
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6722956/
Abstract

Cytochalasans are a group of structurally diverse fungal polyketide-amino acid hybrid metabolites that exhibit diverse biological functions. Asperchalasine A was identified and isolated from an extract of the marine-derived fungus, . Asperchalasine A is a cytochalasan dimer which consists of two cytochalasan molecules connected by an epicoccine. This study investigated the potential antiangiogenic effects of extract and asperchalasine A, which significantly inhibited cell adhesion and tube formation in human umbilical vein endothelial cells (HUVECs). extract and asperchalasine A decreased the vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor (VEGFR)-2 mRNA expression in a concentration-dependent manner. In addition, extract and asperchalasine A inhibited angiogenesis via downregulation of VEGF, p-p38, p-extracellular signal-regulated protein kinase (ERK), p-VEGFR-2, and p-Akt signaling pathways. Moreover, extract and asperchalasine A significantly inhibited the amount of blood vessel formation in fertilized chicken eggs using a chorioallantoic membrane assay. Our results provide experimental evidence of this novel biological activity of the potential antiangiogenic substances, extract, and asperchalasine A. This study also suggests that extract and its active component asperchalasine A are excellent candidates as adjuvant therapeutic substances for cancer prevention and treatment.

摘要

细胞松弛素是一组结构多样的真菌聚酮-氨基酸杂合代谢物，具有多种生物功能。 Asperchalasine A 是从海洋来源的真菌 中鉴定和分离出来的。 Asperchalasine A 是一种细胞松弛素二聚体，由两个细胞松弛素分子通过 epicoccine 连接而成。本研究探讨了 提取物和 asperchalasine A 的潜在抗血管生成作用，它们显著抑制了人脐静脉内皮细胞 (HUVECs) 的细胞黏附和管形成。 提取物和 asperchalasine A 以浓度依赖的方式降低血管内皮生长因子 (VEGF) 和血管内皮生长因子受体 (VEGFR)-2 mRNA 的表达。此外， 提取物和 asperchalasine A 通过下调 VEGF、p-p38、p-细胞外信号调节蛋白激酶 (ERK)、p-VEGFR-2 和 p-Akt 信号通路抑制血管生成。此外， 提取物和 asperchalasine A 在鸡胚绒毛尿囊膜试验中显著抑制了血管生成的数量。我们的研究结果为这种新型生物活性的潜在抗血管生成物质 提取物和 asperchalasine A 提供了实验证据。本研究还表明， 提取物及其活性成分 asperchalasine A 是癌症预防和治疗的辅助治疗物质的良好候选物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/8d5ef813fd3e/biomolecules-09-00358-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/754d409c646b/biomolecules-09-00358-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/b74de0009dc8/biomolecules-09-00358-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/e1384635aca7/biomolecules-09-00358-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/ec866b59a40e/biomolecules-09-00358-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/36dd7bb02c5e/biomolecules-09-00358-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/8baa2b18ea53/biomolecules-09-00358-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/09e8a29b426a/biomolecules-09-00358-g007a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/e55cf4ff3ea6/biomolecules-09-00358-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/8d5ef813fd3e/biomolecules-09-00358-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/754d409c646b/biomolecules-09-00358-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/b74de0009dc8/biomolecules-09-00358-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/e1384635aca7/biomolecules-09-00358-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/ec866b59a40e/biomolecules-09-00358-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/36dd7bb02c5e/biomolecules-09-00358-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/8baa2b18ea53/biomolecules-09-00358-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/09e8a29b426a/biomolecules-09-00358-g007a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/e55cf4ff3ea6/biomolecules-09-00358-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c5f/6722956/8d5ef813fd3e/biomolecules-09-00358-g009.jpg

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