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Page 1 de 497 résultats
Quercetin, a bioflavonoid, inhibits the induction of interleukin 8 and monocyte chemoattractant protein-1 expression by tumor necrosis factor-alpha in cultured human synovial cells.
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OBJECTIVE
Tumor necrosis factor (TNF)-alpha is present in synovial fluid of patients with rheumatoid arthritis. It induces the expression of proinflammatory cytokines in synovial cells. Based on our recent finding that reactive oxygen intermediates play important roles in mediating TNF-alpha action,
Resveratrol more effectively than quercetin reduces endothelium degeneration and level of necrosis factor α in patients with coronary artery disease.
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BACKGROUND
endothelial dysfunction (ED) is one of the most important links in the pathogenesis of atherosclerosis (ASVD) - morphological basis of coronary artery disease (CAD).
OBJECTIVE
to study the effect of polyphenolic antioxidants, resveratrol and quercetin, on endothelial degeneration factors
Sensitization of recombinant human tumor necrosis factor-related apoptosis-inducing ligand-resistant malignant melanomas by quercetin.
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Malignant melanoma is the most commonly diagnosed skin cancer associated with a high rate of metastasis. Low-stage melanoma is easily treated, but metastatic malignant melanoma is an extremely treatment-resistant malignancy with low survival rates. The application of recombinant human tumor necrosis
Activation of phosphatidylinositol 3-kinase is required for tumor necrosis factor-alpha-induced upregulation of matrix metalloproteinase-9: its direct inhibition by quercetin.
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Matrix metalloproteinases (MMPs) are involved in various skin disorders, including photoaging, dermatitis, and tumorigenesis. Tumor necrosis factor (TNF)-alpha is a key proinflammatory cytokine that acts to provoke inflammation, proliferation, and tumorigenesis. The present study investigated the
The effect of quercetin on apoptosis and necrosis induction in human colon adenocarcinoma cell line LS180.
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Quercetin is a very common flavonoid widely distributed in many plants. The flavonoid intake has been linked to the prevention of some human diseases including cancer. Quercetin inhibits heat shock protein expression and in this way triggers apoptosis of tumor cells. The present study was designed
Inhibitory effect of quercetin on tumor necrosis factor and interleukin-1 beta pro-osteoclastic activities.
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OBJECTIVE
To study the effects of quercetin on tumor necrosis factor (TNF) and interleukin-1 beta (IL-1 beta) pro-osteoclastic activities.
METHODS
[3H] TdR uptake by osteoblasts was used to measure cell proliferation, microspectrophotometer for cellular AIP activity using p-nitrophenyl phosphate as
Protective effect of quercetin on the evolution of cisplatin-induced acute tubular necrosis.
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BACKGROUND
The mechanism of cisplatin-induced nephrotoxicity is unknown, but has been associated with renal lipid peroxidation. The bioflavonoid quercetin may be a potential alternative to reduce cisplatin-induced nephrotoxicity. The aim of this study was to evaluate the effect of quercetin on the
Combined Effects of Vincristine and Quercetin in Reducing Isoproterenol-Induced Cardiac Necrosis in Rats.
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Combined effects of vincristine and quercetin in the regulation of isoproterenol (ISO)-induced cardiac necrosis have been evaluated in rats. ISO administration (100 mg/kg, s.c., for two consecutive days) increased the levels of serum creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), glutamate
The Effects of Hesperidin and Quercetin on Serum Tumor Necrosis Factor-Alpha and Interleukin-6 Levels in Streptozotocin-induced Diabetes Model.
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UNASSIGNED
Diabetes mellitus (DM) is a metabolic disorder that occurs as a result of absolute or relative insufficiency of insulin release and/or insulin effect due to impairment of carbohydrate, fat and protein metabolism, and it is characterized by hyperglycemia and leads to various
Quercetin Reduces Tumor Necrosis Factor Alpha-Induced Muscle Atrophy by Upregulation of Heme Oxygenase-1.
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The inflammatory cytokine tumor necrosis factor α (TNFα), upregulated in the obese condition, promotes protein degradation and is implicated in obesity-related skeletal muscle atrophy and age-related sarcopenia. Quercetin, a flavonoid, elicits antioxidative and anti-inflammatory activities. In this
Effects of Ginkgo biloba extract (EGb 761) and quercetin on lipopolysaccharide-induced signaling pathways involved in the release of tumor necrosis factor-alpha.
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Administration of bacterial lipopolysaccharide (LPS) to laboratory animals and cultured macrophages induces tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory cytokine. Pretreatment with Ginkgo biloba extract (EGb 761) inhibited the in vivo production of TNF-alpha (measured by ELISA) after
Quercetin but not quercitrin ameliorates tumor necrosis factor-alpha-induced insulin resistance in C2C12 skeletal muscle cells.
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Skeletal muscle is a major site for glucose metabolism and its injury by cytokines can induce insulin resistance leading to type 2 diabetes. It has been suggested that quercetin may act as an anti-diabetic agent, however, the effects of quercetin on insulin resistance in skeletal muscle remain
The protective effect of quercetin on retinal inflammation in mice: the involvement of tumor necrosis factor/nuclear factor-κB signaling pathways
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Quercetin is a natural flavonoid that occurs in fruits and vegetables. Retinal inflammation is an important cause of vision loss. This study was aimed to analyze the effects of oral administration of quercetin on retinal inflammation. Transgenic mice, carrying nuclear factor-κB (NF-κB)-driven
Quercetin induces necrosis and apoptosis in SCC-9 oral cancer cells.
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Evidence has accumulated that dietary polyphenols, in particular, flavonoids, have protective effects against oral cancer. In this study, we have examined the effects of quercetin, a major dietary flavonoid, on cell growth and necrosis/apoptosis and cell cycle regulation in human oral squamous
Differential activity of kaempferol and quercetin in attenuating tumor necrosis factor receptor family signaling in bone cells.
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Increasing data from epidemiological and in vitro studies show that the isoflavonoids, genistein and daidzein, and the flavonols, quercetin and kaempferol, are protective against postmenopausal bone loss. However, the physiological mechanisms for these effects are not well understood. We now report
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