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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

Substituted trans-stilbenes, including analogues of the natural product resveratrol, inhibit the human tumor necrosis factor alpha-induced activation of transcription factor nuclear factor kappaB.

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The transcription factor nuclear factor kappaB (NF-kappaB), which regulates expression of numerous antiinflammatory genes as well as genes that promote development of the prosurvival, antiapoptotic state is up-regulated in many cancer cells. The natural product resveratrol, a polyphenolic

The anti-inflammatory activity of the polyphenol resveratrol may be partially related to inhibition of tumour necrosis factor-alpha (TNF-alpha) pre-mRNA splicing.

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The present study shows for the first time that the polyphenol resveratrol (RESV) blocks processing of tumour necrosis factor-alpha (TNF-alpha) pre-mRNA in mature mRNA. This study was carried out in turbot (Psetta maxima (L.)), a fish species that we are using to evaluate the effects of RESV on the

Sensitization for tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by the chemopreventive agent resveratrol.

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Survivin is a member of the inhibitor of apoptosis proteins that is expressed at high levels in most human cancers and may facilitate evasion from apoptosis and aberrant mitotic progression. Naturally occurring dietary compounds such as resveratrol have gained considerable attention as cancer

Resveratrol induces apoptotic cell death in rat H4IIE hepatoma cells but necrosis in C6 glioma cells.

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Resveratrol (trans-3,5,4',-trihydroxystilbene) is assumed to possess cancer-preventive and cancer-therapeutic properties. The aim of this project was to analyze cellular effects of resveratrol in metabolically active H4IIE rat hepatoma cells in comparison to metabolically poorly active C6 rat glioma

Production of ex vivo lipopolysaccharide-induced tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 is suppressed by trans-resveratrol in a concentration-dependent manner.

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Trans-resveratrol is a biologically active compound present in certain foods that has anti-inflammatory and anticancer properties. These beneficial effects are derived from both the immune system and cytokines. The purpose of this study was to determine the immunomodulatory effect of

Resveratrol protects primary rat hepatocytes against necrosis induced by reactive oxygen species.

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Reactive oxygen species can be important mediators of damage to cell molecules and structures. Besides the endogen antioxidant defences, the antioxidant intake in the diet has an important role in the protection against the development of diseases produced by oxidative damage. Resveratrol is a

Resveratrol blunts tumor necrosis factor-alpha-induced monocyte adhesion and transmigration.

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The leukocyte recruitment and transmigration across the endothelial barrier into the vessel wall are crucial steps in atherosclerosis. Leukocyte trafficking on the endothelium is elicited by induction of endothelial adhesion molecules, and its transmigration is mediated by degradation of basement

Effects of resveratrol and genistein on nuclear factor‑κB, tumor necrosis factor‑α and matrix metalloproteinase‑9 in patients with chronic obstructive pulmonary disease.

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Chronic airway inflammation and airway remodeling are the major pathophysiological characteristics of chronic obstructive pulmonary disease (COPD). Resveratrol and genistein have been previously demonstrated to have anti‑inflammatory and antioxidative properties. The present study aimed to measure

Resveratrol as a natural anti-tumor necrosis factor-α molecule: implications to dendritic cells and their crosstalk with mesenchymal stromal cells.

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Dendritic cells (DC) are promising targets for inducing tolerance in inflammatory conditions. Thus, this study aims to investigate the effects of the natural anti-inflammatory molecule resveratrol on human DC at phenotypic and functional levels, including their capacity to recruit mesenchymal

Resveratrol suppresses tumor necrosis factor-alpha-induced fractalkine expression in endothelial cells.

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Up-regulation of fractalkine is involved in vascular and tissue damage in inflammatory conditions. Resveratrol has been shown to have anti-inflammatory, antioxidant, and antitumor activities. Its regulatory effects on expression of fractalkine in vascular endothelial cells and fractalkine receptor

Effect of apigenin, kaempferol and resveratrol on the expression of interleukin-1beta and tumor necrosis factor-alpha genes in J774.2 macrophages.

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Flavonoids have been reported to bring benefits in lowering inflammation, oxidative stress and exert positive effects in cancer and cardiovascular and chronic inflammatory diseases. Apigenin, kaempferol and resveratrol present in fruits, vegetables and grain were investigated for their effect on the

Resveratrol and propolis as necrosis or apoptosis inducers in human prostate carcinoma cells.

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Vegetables and fruit help the prevention and the therapy of several kinds of cancer because they contain micronutrients, a class of substances that have been shown to exhibit chemopreventive and chemotherapeutic activities. In the present study the effects of resveratrol (100 and 200 microM), a

Sirtuin-2 activity is required for glioma stem cell proliferation arrest but not necrosis induced by resveratrol.

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Glioblastomas, the most common form of primary brain tumors, are the fourth cause of death by cancer in adults. Increasing evidences suggest that glioblastoma resistance to existing radio- and chemotherapies rely on glioblastoma stem cells (GSCs). GSCs are endowed with a unique combination of

Resveratrol more effectively than quercetin reduces endothelium degeneration and level of necrosis factor α in patients with coronary artery disease.

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