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.
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http://dx.doi.org/10.1038/s41598-017-18069-4 | DOI Listing |
BMC Biotechnol
January 2025
Department of Emergency Medicine, Inner Mongolia People's Hospital, No. 20 Zhaowuda Road, Hohhot City, Inner Mongolia Autonomous Region, 010017, China.
Background: Oxidized low-density lipoprotein (ox-LDL)-induced endothelial cell dysfunction plays a crucial role in the progression of atherosclerosis (AS). Although miR-125b-5p is known to be involved in cardiovascular and cerebrovascular disorders, its function in ox-LDL-induced endothelial injury is still not well understood.
Methods: An in vitro AS cell model was established by exposing human umbilical vein endothelial cells (HUVECs) to 100 µg/mL ox-LDL for 24 h.
Int J Mol Sci
December 2024
Department of Pharmacology, Pharmacy College, Nantong University, Nantong 226001, China.
This research seeks to investigate the function and fundamental mechanisms of Itchy E3 ubiquitin ligase (ITCH), a HECT (homologous to E6AP carboxyl terminus)-type E3 ubiquitin ligase, in endothelial ferroptosis, particularly in the context of atherosclerosis, which has been underexplored. The levels of ITCH protein in the aortas of mice with atherosclerosis were analyzed. Constructs for ITCH RNA interference were generated and introduced into human aortic endothelial cells (HAECs).
View Article and Find Full Text PDFTheranostics
January 2025
Department of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine and Institute of Brain and Brain-Inspired Science, Shandong University, Shandong, China.
Int J Med Microbiol
December 2024
Insititute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, University of South China, Hengyang, Hunan 421001, China. Electronic address:
Cardiovasc Ther
January 2025
Department of Cardiology The First Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
This study is aimed at investigating the effects of atorvastatin (ATV) on endothelial cell injury in atherosclerosis (AS) through inhibiting acyl-CoA synthetase long-chain family member 4 (ACSL4)-mediated ferroptosis. Human umbilical vein endothelial cells (HUVECs) were treated with oxidized low-density lipoprotein (ox-LDL) to establish an in vitro model of AS. The cell viability, lactate dehydrogenase (LDH) release, apoptosis, and expression levels of apoptotic proteins were assessed.
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