scholarly journals Inhibitory Effect of a French Maritime Pine Bark Extract-Based Nutritional Supplement on TNF-α-Induced Inflammation and Oxidative Stress in Human Coronary Artery Endothelial Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Kristine C. Y. McGrath ◽  
Xiao-Hong Li ◽  
Lucinda S. McRobb ◽  
Alison K. Heather
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Cell Adhesion ◽  
Coronary Artery ◽  
Endothelial Dysfunction ◽  
Cell Adhesion Molecule ◽  
Bark Extract ◽  
Human Coronary Artery ◽  
Cell Adhesion Molecule 1 ◽  
And Oxidative Stress

Oxidative stress and inflammation, leading to endothelial dysfunction, contribute to the pathogenesis of atherosclerosis. The popularity of natural product supplements has increased in recent years, especially those with purported anti-inflammatory and/or antioxidant effects. The efficacy and mechanism of many of these products are not yet well understood. In this study, we tested the antioxidant and anti-inflammatory effects of a supplement, HIPER Health Supplement (HIPER), on cytokine-induced inflammation and oxidative stress in human coronary artery endothelial cells (HCAECs). HIPER is a mixture of French maritime pine bark extract (PBE), honey, aloe vera, and papaya extract. Treatment for 24 hours with HIPER reduced TNF-α-induced reactive oxygen species (ROS) generation that was associated with decreased NADPH oxidase 4 and increased superoxide dismutase-1 expression. HIPER inhibited TNF-αinduced monocyte adhesion to HCAECs that was in keeping with decreased expression of vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1 and decreased nuclear factor-kappa B (NF-κB) activation. Further investigation of mechanism showed HIPER reduced TNF-αinduced IκBαand p38 and MEK1/2 MAP kinases phosphorylation. Our findings show that HIPER has potent inhibitory effects on HCAECs inflammatory and oxidative stress responses that may protect against endothelial dysfunction that underlies early atherosclerotic lesion formation.

scholarly journals The Presence of Cholesteryl Ester Transfer Protein (CETP) in Endothelial Cells Generates Vascular Oxidative Stress and Endothelial Dysfunction

Biomolecules ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 69
Author(s):  
Amarylis C. B. A. Wanschel ◽  
Daniele M. Guizoni ◽  
Estela Lorza-Gil ◽  
Alessandro G. Salerno ◽  
Adriene A. Paiva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Cell Adhesion ◽  
Endothelial Dysfunction ◽  
Transgenic Mice ◽  
Cholesteryl Ester Transfer Protein ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Transfer Protein ◽  
Cell Adhesion Molecule 1

Endothelial dysfunction precedes atherosclerosis and is an independent predictor of cardiovascular events. Cholesterol levels and oxidative stress are key contributors to endothelial damage, whereas high levels of plasma high-density lipoproteins (HDL) could prevent it. Cholesteryl ester transfer protein (CETP) is one of the most potent endogenous negative regulators of HDL-cholesterol. However, whether and to what degree CETP expression impacts endothelial function, and the molecular mechanisms underlying the vascular effects of CETP on endothelial cells, have not been addressed. Acetylcholine-induced endothelium-dependent relaxation of aortic rings was impaired in human CETP-expressing transgenic mice, compared to their non-transgenic littermates. However, endothelial nitric oxide synthase (eNOS) activation was enhanced. The generation of superoxide and hydrogen peroxide was increased in aortas from CETP transgenic mice, while silencing CETP in cultured human aortic endothelial cells effectively decreased oxidative stress promoted by all major sources of ROS: mitochondria and NOX2. The endoplasmic reticulum stress markers, known as GADD153, PERK, and ARF6, and unfolded protein response effectors, were also diminished. Silencing CETP reduced endothelial tumor necrosis factor (TNF) α levels, intercellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) expression, diminishing monocyte adhesion. These results support the notion that CETP expression negatively impacts endothelial cell function, revealing a new mechanism that might contribute to atherosclerosis.

Klotho modulates FGF23-mediated NO synthesis and oxidative stress in human coronary artery endothelial cells

2016 ◽  
Vol 468 (9) ◽  
pp. 1621-1635 ◽  
Author(s):  
Beatrice Richter ◽  
Jacqueline Haller ◽  
Dieter Haffner ◽  
Maren Leifheit-Nestler
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Coronary Artery ◽  
Human Coronary Artery ◽  
And Oxidative Stress

Abstract 346: Mice Overexpressing Renin: a New Model of Progressive Chronic Kidney Disease

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Anne-Cecile Huby ◽  
Ahmed Abed ◽  
Panos Kavvadas ◽  
Carlo Alfieri ◽  
Maria-Pia Rastaldi ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Cell Adhesion ◽  
Endothelial Dysfunction ◽  
Kidney Disease ◽  
Renal Disease ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Filtration Barrier ◽  
Human Pathology ◽  
Cell Adhesion Molecule 1

Background: Hypertension-induced chronic kidney disease in mouse models is quite fast and consequently away from the human pathology. There is an increasing need for a mouse model that can be used to delineate the pathogenic process leading to progressive renal disease. Aim: Our objective was dual: to investigate whether mice overexpressing renin ectopically at constant and high levels by genetic clamping (RenTg) could mimic kinetics and the physiopathological characteristics of hypertension-induced CKD and to identify cellular and/or molecular events characterizing the different steps of the progression of CKD. Results: We found that RenTg mice are hypertensive (123±7 vs to 90±2 mm Hg for the wt age-matched animals, p<0.05) and slightly albuminuric (22.1±5.3 vs. 5.2±0.4 g/mol, p<0.01) as early as 3 month old. At this age, the expressions of adhesion markers such as vascular cell adhesion molecule-1 and platelet endothelial cell adhesion molecule-1 are 4-5 fold increased in the renal cortical vasculature indicating the beginning of endothelial dysfunction. Five month-old RenTg mice show perivascular and periglomerular infiltrations of macrophages and their GFR is starting to decrease(-10%). At 8 months, the renal cortex of RenTg mice is altered by leukocyte invasion, decreased expression of nephrin (a protein controlling filtration barrier), increased expression of KIM-1 (a protein typical of tubular cell stress) and of several pro-fibrotic agents of the TGFbeta family, and establishment of fibrotic lesions. At the age of 12 months, RenTg mice display several lesions of renal structure typical of hypertensive renal disease (such as glomerular ischemia, glomerulo- and nephroangio-sclerosis, mesangial expansion, tubular dilation), important proteinuria (138±20 g/mol) and a 55% fall of GFR. Conclusions: The RenTg strain develops progressively with age CKD. In this model, endothelial dysfunction is an early event preceding the structural and fibrotic alterations which ultimately lead to the development of CKD. This model can provide a useful tool allowing to gain new insights into the mechanisms of chronic renal failure and to identify new targets for arresting and/or reversing the development of CKD

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