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天麻素通过上调 miR-21 促进人脐静脉内皮细胞的血管生成能力，激活 PI3K/Akt 信号通路。

The up-regulation of miR-21 by gastrodin to promote the angiogenesis ability of human umbilical vein endothelial cells by activating the signaling pathway of PI3K/Akt.

机构信息

Department Of Neurology, Affiliated Hospital Of Nanjing University Of Chinese Medicine, Nanjing, China.

Department Of Neurology, Jiangsu Province Hospital Of Chinese Medicine, Nanjing, China.

出版信息

Bioengineered. 2021 Dec;12(1):5402-5410. doi: 10.1080/21655979.2021.1964895.

DOI:10.1080/21655979.2021.1964895
PMID:34424813
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8806924/
Abstract

Studies have shown that gastrodin has a protective effect on blood vessels. The purpose of this study was to investigate the influence of gastrodin on the angiogenesis ability of human umbilical vein endothelial cells (HUVECs) and its mechanism. We found that treatment of HUVECs with 10 µM and 25 µM gastrodin, and Vascular endothelial growth factor (VEGF) significantly upregulated the miR-21 expression in the cells. Meanwhile, gastrodin significantly increased the cell proliferation, migration and tube formation ability of HUVECs and increased the expression of MMP-2 and MMP-9 mRNA. In addition, gastrodin promoted the phosphorylation level of PI3K/Akt protein. However, down-regulating the miR-21 expression reduced the promoting effect of gastrodin on the HUVECs angiogenesis. In conclusion, gastrodin activates the PI3K/Akt pathway by up-regulating the miR-21 expression and promotes the HUVECs angiogenesis.

摘要

研究表明天麻素对血管具有保护作用。本研究旨在探讨天麻素对人脐静脉内皮细胞（HUVEC）血管生成能力的影响及其机制。我们发现，10μM 和 25μM 天麻素和血管内皮生长因子（VEGF）处理 HUVEC 可显著上调细胞中 miR-21 的表达。同时，天麻素可显著增加 HUVEC 的细胞增殖、迁移和管腔形成能力，并增加 MMP-2 和 MMP-9 mRNA 的表达。此外，天麻素促进了 PI3K/Akt 蛋白的磷酸化水平。然而，下调 miR-21 的表达可降低天麻素对 HUVEC 血管生成的促进作用。总之，天麻素通过上调 miR-21 的表达激活 PI3K/Akt 通路，促进 HUVEC 血管生成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bebc/8806924/45f7b4ac9542/KBIE_A_1964895_F0005_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bebc/8806924/c1005a1c034e/KBIE_A_1964895_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bebc/8806924/ae0586b86ebe/KBIE_A_1964895_F0002_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bebc/8806924/1c63a276f00b/KBIE_A_1964895_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bebc/8806924/c2c1551a335c/KBIE_A_1964895_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bebc/8806924/45f7b4ac9542/KBIE_A_1964895_F0005_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bebc/8806924/c1005a1c034e/KBIE_A_1964895_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bebc/8806924/ae0586b86ebe/KBIE_A_1964895_F0002_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bebc/8806924/1c63a276f00b/KBIE_A_1964895_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bebc/8806924/c2c1551a335c/KBIE_A_1964895_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bebc/8806924/45f7b4ac9542/KBIE_A_1964895_F0005_B.jpg

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