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Effect of resveratrol derivative BTM-0512 on high glucose-induced dysfunction of endothelial cells: role of SIRT1.
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- Author(s): Yuan Q;Yuan Q; Chen L; Xiang DX; Li YJ; Hu CP
- Source:
Canadian journal of physiology and pharmacology [Can J Physiol Pharmacol] 2011 Oct; Vol. 89 (10), pp. 713-22. Date of Electronic Publication: 2011 Sep 09.
- Publication Type:
Journal Article; Research Support, Non-U.S. Gov't
- Language:
English
- Additional Information
- Source:
Publisher: Canadian Science Publishing Country of Publication: Canada NLM ID: 0372712 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1205-7541 (Electronic) Linking ISSN: 00084212 NLM ISO Abbreviation: Can J Physiol Pharmacol Subsets: MEDLINE
- Publication Information:
Publication: 2011- : Ottawa, ON : Canadian Science Publishing
Original Publication: Ottawa, National Research Council of Canada.
- Subject Terms:
- Abstract:
Hyperglycemia impairs the function of endothelial cells. Sirtuin 1 (SIRT1) is involved in regulating the function of endothelial cells. Resveratrol, a polyphenol found in many plant species, exerts protective effects on endothelial cells through activation of SIRT1. The aims of this work were to explore whether BTM-0512, a novel derivative of resveratrol, is able to exert beneficial effects on high glucose-induced dysfunction of endothelial cells through regulation of SIRT1. We found that high glucose significantly impaired the function of endothelial cells as shown by reduced tube formation, cell migration, and cell adhesion concomitantly with downregulation of mRNA expression of SIRT1 and vascular endothelial growth factor as well as increased tumor necrosis factor-α release and reactive oxygen species production. These effects of high glucose were inhibited by pretreatment with BTM-0512. The beneficial effects of BTM-0512 on high glucose-induced cell dysfunction were abolished by splitomicin, a specific inhibitor of SIRT1. The regulatory effects of BTM-0512 on high glucose-induced changes in vascular endothelial growth factor mRNA expression and tumor necrosis factor-α release were also abolished by splitomicin. The results suggest that BTM-0512 exerts beneficial effects on high glucose-induced endothelial cell dysfunction through regulation of the SIRT1 - reactive oxygen species - vascular endothelial growth factor - tumor necrosis factor-α pathway.
- Accession Number:
0 (3,4',5-trimethoxystilbene)
0 (Antioxidants)
0 (Reactive Oxygen Species)
0 (Stilbenes)
0 (Tumor Necrosis Factor-alpha)
0 (Vascular Endothelial Growth Factor A)
EC 3.5.1.- (SIRT1 protein, human)
EC 3.5.1.- (Sirtuin 1)
IY9XDZ35W2 (Glucose)
Q369O8926L (Resveratrol)
- Publication Date:
Date Created: 20110913 Date Completed: 20120203 Latest Revision: 20181201
- Publication Date:
20240829
- Accession Number:
10.1139/y11-069
- Accession Number:
21905824
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