Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/87564
Title: Proteomic investigation of effects of hydroxysafflor yellow A in oxidized low-density lipoprotein-induced endothelial injury
Authors: Ye, Feng
Wang, Jianhe
Meng, Wei
Qian, Jingru
Jin, Ming
Keywords: Oxidized
Endothelial Injury
Issue Date: 2017
Source: Ye, F., Wang, J., Meng, W., Qian, J., & Jin, M. (2017). Proteomic investigation of effects of hydroxysafflor yellow A in oxidized low-density lipoprotein-induced endothelial injury. Scientific Reports, 7(1), 17981-.
Series/Report no.: Scientific Reports
Abstract: Oxidized low-density lipoprotein (ox-LDL)-induced vascular endothelial damage is a key event in early atherosclerosis. Safflower has been used to treat atherosclerotic heart disease in China for many years, but its molecular basis remains unclear. Hydroxysafflor yellow A (HSYA) is the main active ingredient of aqueous safflower extract. We identified the proteins involved in HSYA activity against ox-LDL-induced endothelial injury using isobaric tags for relative and absolute quantification-coupled two-dimensional liquid chromatography–tandem mass spectrometry. HSYA (1, 5, or 25 μM) alleviated ox-LDL-induced endothelial damage in a dose-dependent manner. We quantitated approximately 2700 protein species, of which 77 were differentially expressed following HSYA treatment. Most protein changes were related to structural molecules, metabolic enzymes, and proteins involved in signal transduction. Several differentially expressed proteins were further validated by western blot analysis. We also analysed the role of the mitochondrial membranous voltage-dependent anion-selective channel protein 2 (VDAC2) in HSYA treatment using small interfering RNA. VDAC2 functioned as a downstream anti-apoptosis effector during HSYA treatment of ox-LDL-induced endothelial impairment. These results further our understanding of the mechanisms responsible for the effects of HSYA.
URI: https://hdl.handle.net/10356/87564
http://hdl.handle.net/10220/45402
ISSN: 2045-2322
DOI: http://dx.doi.org/10.1038/s41598-017-18069-4
Rights: © 2017 The Author(s) (Nature Publishing Group). This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
metadata.item.grantfulltext: open
metadata.item.fulltext: With Fulltext
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