scholarly journals Nanoencapsulation of the omega-3 EPA:DHA 6:1 formulation enhances and sustains NO-mediated endothelium-dependent relaxations in coronary artery rings and NO formation in endothelial cells

2021 ◽  
Vol 87 ◽  
pp. 104851
Author(s):  
L. Remila ◽  
E. Belcastro ◽  
N. Guenday-Tuereli ◽  
S. Park ◽  
U. Houngue ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Coronary Artery ◽  
Omega 3 ◽  
No Formation

Inhibition of Pro-Inflammatory Cytokine Secretion by Select Antioxidants in Human Coronary Artery Endothelial Cells

2020 ◽  
Vol 90 (1-2) ◽  
pp. 103-112 ◽  
Author(s):  
Michael J. Haas ◽  
Marilu Jurado-Flores ◽  
Ramadan Hammoud ◽  
Victoria Feng ◽  
Krista Gonzales ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Ascorbic Acid ◽  
Coronary Artery ◽  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Culture Media ◽  
Cytokine Secretion ◽  
Human Coronary Artery ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

Abstract. Inflammatory and oxidative stress in endothelial cells are implicated in the pathogenesis of premature atherosclerosis in diabetes. To determine whether high-dextrose concentrations induce the expression of pro-inflammatory cytokines, human coronary artery endothelial cells (HCAEC) were exposed to either 5.5 or 27.5 mM dextrose for 24-hours and interleukin-1β (IL-1β), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor α (TNF α) levels were measured by enzyme immunoassays. To determine the effect of antioxidants on inflammatory cytokine secretion, cells were also treated with α-tocopherol, ascorbic acid, and the glutathione peroxidase mimetic ebselen. Only the concentration of IL-1β in culture media from cells exposed to 27.5 mM dextrose increased relative to cells maintained in 5.5 mM dextrose. Treatment with α-tocopherol (10, 100, and 1,000 μM) and ascorbic acid (15, 150, and 1,500 μM) at the same time that the dextrose was added reduced IL-1β, IL-6, and IL-8 levels in culture media from cells maintained at 5.5 mM dextrose but had no effect on IL-1β, IL-6, and IL-8 levels in cells exposed to 27.5 mM dextrose. However, ebselen treatment reduced IL-1β, IL-6, and IL-8 levels in cells maintained in either 5.5 or 27.5 mM dextrose. IL-2 and TNF α concentrations in culture media were below the limit of detection under all experimental conditions studied suggesting that these cells may not synthesize detectable quantities of these cytokines. These results suggest that dextrose at certain concentrations may increase IL-1β levels and that antioxidants have differential effects on suppressing the secretion of pro-inflammatory cytokines in HCAEC.

scholarly journals Omega-3 Fatty Acid Supplementation Does Not Reduce Risk of Atrial Fibrillation After Coronary Artery Bypass Surgery

2010 ◽  
Vol 3 (1) ◽  
pp. 46-53 ◽  
Author(s):  
Palaniappan Saravanan ◽  
Ben Bridgewater ◽  
Annette L. West ◽  
Stephen C. O'Neill ◽  
Philip C. Calder ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Fatty Acid ◽  
Coronary Artery ◽  
Coronary Artery Bypass Surgery ◽  
Bypass Surgery ◽  
Artery Bypass ◽  
Omega 3 ◽  
Fatty Acid Supplementation ◽  
Omega 3 Fatty Acid ◽  
Reduce Risk

scholarly journals Neutrophil-endothelial cells modulation in diabetic patients undergoing coronary artery bypass grafting

1998 ◽  
Vol 14 (4) ◽  
pp. 373-379 ◽  
Author(s):  
Massimo Chello ◽  
Pasquale Mastroroberto ◽  
Francesco Cirillo ◽  
E. Bevacqua ◽  
Antonio Carrano ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Coronary Artery ◽  
Coronary Artery Bypass Grafting ◽  
Coronary Artery Bypass ◽  
Artery Bypass ◽  
Diabetic Patients ◽  
Bypass Grafting ◽  
Artery Bypass Grafting

scholarly journals Infection of Human Coronary Artery Endothelial Cells by Group B Streptococcus Contributes to Dysregulation of Apoptosis, Hemostasis, and Innate Immune Responses

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Claudia Beyrich ◽  
Jürgen Löffler ◽  
Anna Kobsar ◽  
Christian P. Speer ◽  
Susanne Kneitz ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Coronary Artery ◽  
Group B Streptococcus ◽  
Gene Array ◽  
Neonatal Morbidity ◽  
Innate Immune ◽  
Human Coronary Artery ◽  
Chemotactic Protein ◽  
Early Onset Sepsis ◽  
Group B

Early onset sepsis due to group B streptococcus leads to neonatal morbidity, increased mortality, and long-term neurological deficencies. Interaction between septicemic GBS and confluent monolayers of human coronary artery endothelial cells (HCAECs) was analyzed by genome wide expression profiling. In total, 124 genes were differentially expressed (89 upregulated, 35 downregulated) based on a more than 3-fold difference to control HCAEC. Regulated genes are involved in apoptosis, hemostasis, oxidative stress response, infection, and inflammation. Regulation of selected genes and proteins identified in the gene array analysis was confirmed by Real-time RT-PCR assay (granulocyte chemotactic protein 2), ELISA (urokinase, cyclooxygenase 2, granulocyte chemotactic protein 1), and western blotting (Heme oxygenase1, BCL2 interacting protein) at various time points between 4 and 24 hours. These results indicate that GBS infection might influence signalling pathways leading to impaired function of the innate immune system and hemorrhagic and inflammatory complications during GBS sepsis.

N-arachidonylethanolamide relaxation of bovine coronary artery is not mediated by CB1 cannabinoid receptor

1998 ◽  
Vol 274 (1) ◽  
pp. H375-H381 ◽  
Author(s):  
Phillip F. Pratt ◽  
Cecilia J. Hillard ◽  
William S. Edgemond ◽  
William B. Campbell
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Acid Amide ◽  
Cb1 Receptor ◽  
Isometric Tension ◽  
A 23187 ◽  
Sr 141716A ◽  
Rat Mesenteric Artery

It has been reported that the endogenous cannabinoid N-arachidonylethanolamide (AEA), commonly referred to as anandamide, has the characteristics of an endothelium-derived hyperpolarizing factor in rat mesenteric artery. We have carried out studies to determine whether AEA affects coronary vascular tone. The vasorelaxant effects of AEA were determined in isolated bovine coronary artery rings precontracted with U-46619 (3 × 10−9 M). AEA decreased isometric tension, producing a maximal relaxation of 51 ± 9% at a concentration of 10−5 M. Endothelium-denuded coronary arteries were not significantly affected by AEA. The CB1 receptor antagonist SR-141716A (10−6 M) failed to reduce the vasodilatory effects of AEA, suggesting that the CB1 receptor is not involved in this action of AEA. Because AEA is rapidly converted to arachidonic acid and ethanolamine in brain and liver by a fatty acid amide hydrolase (FAAH), we hypothesized that the vasodilatory effect of AEA results from its hydrolysis to arachidonic acid followed by enzymatic conversion to vasodilatory eicosanoids. In support of this hypothesis, bovine coronary arteries incubated with [3H]AEA for 30 min hydrolyzed 15% of added substrate; ∼9% of the radiolabeled product was free arachidonic acid, and 6% comigrated with the prostaglandins (PGs) and epoxyeicosatrienoic acids (EETs). A similar result was obtained in cultured bovine coronary endothelial cells. Inhibition of the FAAH with diazomethylarachidonyl ketone blocked both the metabolism of [3H]AEA and the relaxations to AEA. Whole vessel and cultured endothelial cells prelabeled with [3H]arachidonic acid synthesized [3H]PGs and [3H]EETs, but not [3H]AEA, in response to A-23187. Furthermore, SR-141716A attenuated A-23187-stimulated release of [3H]arachidonic acid, suggesting that it may have actions other than inhibition of CB1 receptor. These experiments suggest that AEA produces endothelium-dependent vasorelaxation as a result of its catabolism to arachidonic acid followed by conversion to vasodilatory eicosanoids such as prostacyclin or the EETs.

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