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eicosapentaenoic acid/hypoxia
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The effects of long-term treatment with eicosapentaenoic acid and docosahexaenoic acid on hypoxia/rexoygenation injury of isolated cardiac cells in adult rats.
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N-3 polyunsaturated fatty acids have been epidemiologically demonstrated to decrease the incidence of ischaemic heart disease. The present study was undertaken to examine the effects of long-term treatment with eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on hypoxia/reoxygenation
Effects of long-term treatment with eicosapentaenoic acid on the heart subjected to ischemia/reperfusion and hypoxia/reoxygenation in rats.
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The effects of eicosapentaenoic acid (EPA) and long-term treatment with EPA-ethylester (EPA-E) were examined in perfused rat hearts subjected to ischemia/reperfusion and adult rat cardiomyocytes subjected to hypoxia/reoxygenation. EPA (0.1 microM) improved postischemic contractile dysfunction of the
Long-term supplementation with eicosapentaenoic acid salvages cardiomyocytes from hypoxia/reoxygenation-induced injury in rats fed with fish-oil-deprived diet.
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Dietary supplementation of fish oil containing eicosapentaenoic acid (C20:5 n-3, EPA) and docosahexaenoic acid (C22:6 n-3, DHA) has been shown to exert protective effects on ischemic/reperfused hearts. We determined whether deprivation of fish oil from the diet paradoxically enhances susceptibility
Pretreatment with eicosapentaenoic acid prevented hypoxia/reoxygenation-induced abnormality in endothelial gap junctional intercellular communication through inhibiting the tyrosine kinase activity.
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Eicosapentaenoic acid (EPA) may protect against atherosclerotic disease, and modulation of endothelium function is one possible mechanism. Hypoxia/reoxygenation (H/R) is a potential risk factor for the pathogenesis of atherosclerosis, and it causes endothelial dysfunction. To evaluate whether EPA
Eicosapentaenoic acid protects endothelial cell function injured by hypoxia/reoxygenation.
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Eicosapentaenoic acid (EPA) may protect against atherosclerosis by improving lipid metabolism and modulating vascular cell function. Ischemia/ reperfusion injury is one risk factor for atherosclerosis. We investigated if EPA could improve hypoxia/reoxygenation (H/R)-induced endothelial cell
Inhibitory effects of eicosapentaenoic acid (EPA) on the hypoxia/reoxygenation-induced tyrosine kinase activation in cultured human umbilical vein endothelial cells.
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We have previously reported that the n-3 polyunsaturated fatty acid eicosapentaenoic acid (EPA) inhibited the abnormal gap junctional intercellular communication (GJIC) induced by hypoxia/reoxygenation (H/R) via suppressing tyrosine kinase (TK) activation (Zhang et al., Prostaglandins Leukot Essent
Could omega-3 fatty acids a therapeutic treatment of the immune-metabolic consequence of intermittent hypoxia in obstructive sleep apnea?
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Obesity and Obstructive sleep Apnea (OSA) seems to bi-directional; obesity itself increases the risk of OSA, but on the other hand, OSA may also predispose the individuals to weight gain, both obesity and OSA share a common immune-metabolic link state which have a synergistic effect on the
Influence of phospholipid long chain polyunsaturated fatty acid composition on neonatal rat cardiomyocyte function in physiological conditions and during glucose-free hypoxia-reoxygenation.
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There is evidence that dietary polyunsaturated fatty acids (PUFA) may protect against cardiovascular diseases, but the involvement of the cardiac muscle cell in this beneficial action remain largely unknown. The present study compared the respective influence of n-3 and n-6 PUFA on the function of
Effect of arachidonic acid metabolic inhibitors on hypoxia/reoxygenation-induced renal cell injury.
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The present study was undertaken to examine the role of arachidonic acid (AA) metabolites in hypoxia/reoxygenation (H/R)-induced renal cell injury in rabbit renal cortical slices using AA metabolic inhibitors. Inhibitors of cyclooxygenase (indomethacin and diclofenac sodium) and lipoxygenase
Effects of oral eicosapentaenoic acid versus docosahexaenoic acid on human peripheral blood mononuclear cell gene expression.
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OBJECTIVE
Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have beneficial effects on inflammation and cardiovascular disease (CVD). Our aim was to assess the effect of a six-week supplementation with either olive oil, EPA, or DHA on gene expression in peripheral blood mononuclear cells
Eicosanoid synthesis in cardiomyocytes: influence of hypoxia, reoxygenation, and polyunsaturated fatty acids.
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The synthesis of eicosanoids was investigated in cultured rat ventricular myocytes. Under normoxia, the cardiomyocytes released 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) and prostaglandin (PG) E2 and smaller amounts of PGF2 alpha and thromboxane B2. Hypoxia enhanced the production of PGE2 and
Eicosapentaenoic and docosahexaenoic acids in cultured rat ventricular myocytes and hypoxia-induced alterations of phospholipase-A activity.
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Hypoxia was reported to induce a decrease in phosphatidylcholine-hydrolyzing phospholipase activity (PC-PLA) in cultured rat cardiomyocytes. This work was intended to compare the influence of the presence of either eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) in the phospholipids on the
Small molecules exert anti-apoptotic effect and reduce oxidative stress augmenting insulin secretion in stem cells engineered islets against hypoxia.
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Transplantation of pancreatic islets is the most reliable treatment for Type 1 diabetes. However cell death mediated by hypoxia is considered as one of the main difficulties hindering success in islet transplantation. The aim of our experiment was to investigate the role of small molecules in
Fatty acids and hypoxia stimulate the expression and secretion of the adipokine ANGPTL4 (angiopoietin-like protein 4/ fasting-induced adipose factor) by human adipocytes.
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OBJECTIVE
Hypoxia occurs in white adipose tissue in obesity, modulating the expression and release of specific inflammation-related adipokines. ANGPTL4 (angiopoietin-like protein 4/fasting-induced adipose factor), which is implicated in angiogenesis, lipid metabolism and glucose homeostasis, is a
Maternal eicosapentaenoic acid feeding promotes placental angiogenesis through a Sirtuin-1 independent inflammatory pathway.
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Maternal overnutrition or obesity is associated with a wide range of metabolic disorders and may impair placental angiogenesis. Previous studies have shown that n-3 polyunsaturated fatty acids (PUFA) promote fetal growth in both rodents and humans. Whether n-3 PUFA impacts on placental angiogenesis
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