Influence of Delphinidin-3-glucoside on Oxidized Low-Density Lipoprotein-Induced Oxidative Stress and Apoptosis in Cultured Endothelial Cells

2012 ◽  
Vol 60 (7) ◽  
pp. 1850-1856 ◽  
Author(s):  
Xueping Xie ◽  
Ruozhi Zhao ◽  
Garry X. Shen
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Cultured Endothelial Cells

Induction of glutathione synthesis by oxidized low-density lipoprotein and 1-palmitoyl-2-arachidonyl phosphatidylcholine: protection against quinone-mediated oxidative stress

2002 ◽  
Vol 362 (1) ◽  
pp. 51-59 ◽  
Author(s):  
Douglas R. MOELLERING ◽  
Anna-Liisa LEVONEN ◽  
Young-Mi GO ◽  
Rakesh P. PATEL ◽  
Dale A. DICKINSON ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Polar Lipid ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Oxidation Products ◽  
Regulatory Subunit ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Increased Activity

Exposure of endothelial cells to oxidized low-density lipoprotein (oxLDL) leads to diverse cellular effects, including induction of the intracellular antioxidant GSH. It is not known whether lipid-or protein-derived oxidation products cause GSH induction and whether this involves increased activity of the key enzyme in its synthesis, glutamate—cysteine ligase (GCL). Furthermore, the effect of oxLDL exposure on the cell's ability to combat oxidative stress has not been previously examined. In the present study we found that, in bovine aortic endothelial cells, LDL or 1-palmitoyl-2-arachidonyl phosphatidylcholine oxidized by different reactive oxygen and nitrogen species induced GSH synthesis. However, prevention of GSH synthesis during exposure to oxLDL caused extensive cell death. The mediator causing GSH induction was shown to be a polar lipid and resulted in the increased activity of GCL as well as increased protein levels of the regulatory subunit of GCL. Pretreatment with both oxLDL and the polar lipid subfraction of the oxLDL protected cells against the toxicity of 2,3-dimethoxynaphthoquinone (DMNQ), a superoxide- and H2O2-forming compound. The potential of a low level of lipid peroxidation products to initiate cytoprotective pathways are discussed.

scholarly journals Circ_0004104 knockdown alleviates oxidized low-density lipoprotein-induced dysfunction in vascular endothelial cells through targeting miR-328-3p/TRIM14 axis in atherosclerosis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Chi Zhang ◽  
Liyue Wang ◽  
Ying Shen
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Cell Viability ◽  
Vascular Endothelial Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Luciferase Reporter ◽  
Low Density ◽  
Vascular Endothelial ◽  
Oxidized Low Density Lipoprotein

Abstract Background Circular RNAs have shown important regulatory roles in cardiovascular diseases, containing atherosclerosis (AS). We intended to explore the role of circ_0004104 in AS using oxidized low-density lipoprotein (ox-LDL)-induced vascular endothelial cells and its associated mechanism. Methods Real-time quantitative polymerase chain reaction and Western blot assay were conducted to analyze RNA levels and protein levels, respectively. Cell viability, apoptosis, angiogenic ability and inflammatory response were assessed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay, flow cytometry, capillary-like network formation assay and enzyme-linked immunosorbent assay, respectively. Cell oxidative stress was assessed using commercial kits. Dual-luciferase reporter assay, RNA immunoprecipitation assay and RNA-pull down assay were performed to verify the intermolecular interaction. Results ox-LDL exposure up-regulated the level of circ_0004104 in HUVECs. ox-LDL exposure suppressed cell viability and angiogenic ability whereas promoted the apoptosis, inflammation and oxidative stress of HUVECs partly through up-regulating circ_0004104. MicroRNA-328-3p (miR-328-3p) was confirmed as a target of circ_0004104. MiR-328-3p interference largely reversed circ_0004104 silencing-mediated effects in HUVECs upon ox-LDL exposure. MiR-328-3p interacted with the 3′ untranslated region of tripartite motif 14, and circ_0004104 positively regulated TRIM14 expression by sponging miR-328-3p. TRIM14 overexpression largely overturned miR-328-3p accumulation-induced influences in HUVECs upon ox-LDL exposure. Conclusion Circ_0004104 knockdown attenuated ox-LDL-induced dysfunction in HUVECs via miR-328-3p-mediated regulation of TRIM14.

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