scholarly journals Zedoarondiol Attenuates Endothelial Cells Injury Induced by Oxidized Low-Density Lipoprotein via Nrf2 Activation

2018 ◽  
Vol 48 (4) ◽  
pp. 1468-1479 ◽  
Author(s):  
Huimin Mao ◽  
Tianqi Tao ◽  
Xiaoren Wang ◽  
Mi Liu ◽  
Dandan Song ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Protective Effect ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Cell Counting ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Sod Activity ◽  
Tnf Α

Background/Aims: Zedoarondiol, a sesquiterpene lactone compound, showed an anti-proliferative activity on vascular smooth muscle cells in our previous study. However, whether it has a beneficial effect on endothelial cells injury induced by oxidized low-density lipoprotein (ox-LDL) remains unclear. This study was designed to investigate the protective effect of zedoarondiol on ox-LDL-induced injury of endothelial cells and explored its underlying mechanism. Methods: The protective effect of zedoarondiol on ox-LDL-induced human umbilical vein endothelial cells (HUVECs) injury were evaluated by Cell Counting Kit-8 (CCK-8) assay and released lactic dehydrogenase (LDH) activity assay. Oxidative stress was determined by malonedialdehyde (MDA) content and superoxide dismutase (SOD) activity. The level of reactive oxygen species (ROS) was measured by dichlorodihydrofluorescin diacetate (DCFH-DA) staining. The culture supernatant was collected for enzyme linked immune-sorbent assays (ELISA) of interleukine-1β (IL-1β), tumor necrosis factor-α (TNF-α), and monocyte chemoattractant protein-1 (MCP-1). Immunofluorescence staining was used to observe NF-E2-related factor 2 (Nrf2) translocation. Western blotting was performed to determine the expression of IL-1β, TNF-α, MCP-1, Kelch-like ECH associated protein 1 (Keap1), heme oxygenase-1 (HO-1), NAD(P)H: quinone oxidoreductase-1 (NQO1), and Nrf2. Results: Zedoarondiol attenuated HUVECs injury, up-regulated SOD activity, suppressed formation of MDA and ROS, and secretion and protein expression of IL-1β, TNF-α, and MCP-1 in injured HUVECs induced by ox-LDL. Zedoarondiol induced nuclear Nrf2 translocation from cytoplasm into nucleus and up-regulated expression of HO-1, NQO1, and Nrf2 in nucleus. All-trans-retinoic acid (ATRA), an inhibitor of Nrf2, abolished zedoarondiol-mediated anti-oxidative effect. Conclusion: Zedoarondiol attenuates ox-LDL-induced endothelial cells injury by inhibiting oxidative stress and inflammation via Nrf2/HO-1 pathway, suggesting that zedoarondiol might be meaningful on prevention and treatment of atherosclerosis.

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.

Extracts of Paris Polyphylla Smith Mitigates Oxidative Stress in Human Umbilical Vein Endothelial Cells Induced by Oxidized Low Density Lipoprotein

2011 ◽  
Vol 365 ◽  
pp. 348-353
Author(s):  
Lin Lin Gao ◽  
Fu Rong Li ◽  
Yan Hong Si ◽  
Shu Cun Qin
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Umbilical Vein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Human Umbilical Vein ◽  
Paris Polyphylla ◽  
Umbilical Vein Endothelial Cells

Paris Polyphylla Smith is widely used in traditional Chinese medicine. For its effective of antipyretic detoxicate, its active component is steroid saponin[1]. The present study was designed to evaluate the antioxidative effect of extracts of Paris Polyphylla Smith (PPSE) and its capacity to protect human umbilical vein endothelial cells (HUVECs) against oxidative damage induced by oxidized low density lipoprotein (ox-LDL). Cytotoxicity was determined by MTT assay. Flow cytometer (FCM) demonstrated that the increased apoptosis induced by oxidized low density were inhibited, and the blocked transition of cells from static phase (G0/G1) to DNA synthesis (S) were restored by PPSE, these effect were all in a dose-dependent manner. The actions by PPSE to reduce apoptosis may help protect endothelial function and inhibit atherogenesis, while the novel actions to mitigates oxidative stress may weaken the ability of endothelial injury. Further studies are needed to identify the chemical compounds responsible in order to develop its clinical application.

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