flavone/necrotisch

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Flavone of Hippophae (H-flavone) lowers atherosclerotic risk factors via upregulation of the adipokine C1q/tumor necrosis factor-related protein 6 (CTRP6) in macrophages.

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In this study, we examined the mechanism of Flavone of Hippophae (H-flavone) in regulating macrophage foaming and atherosclerosis (AS) plaque formation. H-flavone treatment increased the secretion of C1q/tumor necrosis factor-related proteins 6 (CTRP6) in Ox-LDL-treated mouse peripheral blood

[Effects of flavone from leaves of Diospyros kaki on expression of apoptosis signal-regulating kinase 1 and rat vascular smooth muscle cells proliferation by tumor necrosis factor alpha in vitro].

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OBJECTIVE To observe the effects of flavone from leaves of Diospyros kaki on expression of apoptosis signal-regulating kinase 1 (ASK1) and rat vascular smooth muscle cells (VSMCs) proliferation by tumor necrosis factor alpha in vitro. METHODS Rat aortic VSMCs were cultured in vitro and treated with

Polymethoxylated flavones derived from citrus suppress tumor necrosis factor-alpha expression by human monocytes.

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Flavonoids isolated from citrus were evaluated for their ability to affect the inflammation response through suppression of cytokine expression by human monocytes. Several polymethoxylated flavones inhibited lipopolysaccharide-induced monocyte expression of tumor necrosis factor (TNFalpha).

Flavone acetic acid potentiates the induction of endothelial procoagulant activity by tumour necrosis factor.

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Treatment of human umbilical vein endothelial cells with flavone acetic acid (FAA) at 800 micrograms/ml for 4 h resulted in a 3-11-fold increase in procoagulant activity. This increase was due to enhanced tissue factor expression on the endothelial cell surface, as evidenced by the blocking of the

In vivo effects of tumor necrosis factor-alpha or flavone acetic acid in combination with doxorubicin on multidrug-resistant B16 melanoma.

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Having observed that tumor necrosis factor (TNF)-alpha and doxorubicin (DXR) produce a synergistic inhibition of melanoma B16 and also of its multidrug resistant (MDR) variant in vitro, we tested whether this interaction would occur in vivo as well. C57BL/6 mice with s.c. tumors were treated with

Flavone acetic acid and 5,6-dimethylxanthenone-4-acetic acid: relationship between plasma nitrate elevation and the induction of tumour necrosis.

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Antitumour agents such as flavone acetic acid, xanthenone acetic acid (XAA), 5,6-dimethylxanthenone-4-acetic acid and tumour necrosis factor-alpha, following single dose administration to mice with colon 38 adenocarcinomas, induce tumour haemorrhagic necrosis and an elevation in plasma nitrate. The

Tumour necrosis factor-alpha plasma levels after flavone acetic acid administration in man and mouse.

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Flavone acetic acid (FAA) is a synthetic flavonoid with a remarkable spectrum of anticancer activities in mouse tumours, but with no anticancer activity in humans. The mechanism of action of this drug is complex and involves a tumour vasculature action similar to the effects of tumour necrosis

Induction of tumor necrosis factor-alpha messenger RNA in human and murine cells by the flavone acetic acid analogue 5,6-dimethylxanthenone-4-acetic acid (NSC 640488).

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The investigational antitumor agent, 5,6-dimethylxanthenone-4-acetic acid (5,6-MeXAA; NSC 640488) induced greater expression of tumor necrosis factor-alpha (TNF-alpha) mRNA in murine spleen cells in vivo at its optimal dose of 27.5 mg/kg than flavone acetic acid (FAA; NSC 347512) at its optimal dose

Role of T cells and tumour necrosis factor in antitumour activity and toxicity of flavone acetic acid.

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To investigate the importance of natural killer (NK) and T cells in the inhibition of tumour growth by flavone acetic acid (FAA), colon 26 murine carcinoma was grafted subcutaneously in euthymic and athymic mice. FAA was active in euthymic but not in athymic mice (ratio between tumour weight in

Effect of flavone acetic acid (NSC 347,512) on splenic cytotoxic effector cells and their role in tumour necrosis.

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Flavone acetic acid (FAA), an antitumour agent currently undergoing clinical trial, has immune-modulatory effects on various cytotoxic cells in mice. Natural killer (NK) cell activity in the spleen was augmented 4 h after FAA treatment, and when spleen cells were cultured with interleukin-2 to

Comparison of the effects of flavone acetic acid, fostriecin, homoharringtonine and tumour necrosis factor alpha on colon 38 tumours in mice.

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Advanced subcutaneous Colon 38 tumours in mice were used for the assessment of activity of a number of anticancer drugs. Activity was measured by histological examination of tumours 24 h after a single dose of the drug and in some cases by tumour growth delay. Agents thought to exert their cytotoxic

Wogonin and related natural flavones overcome tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) protein resistance of tumors by down-regulation of c-FLIP protein and up-regulation of TRAIL receptor 2 expression.

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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising anticancer agent that kills various tumor cells without damaging normal tissues. However, many cancers remain resistant to TRAIL. To overcome TRAIL resistance, combination therapies using sensitizers of the TRAIL pathway

Role of tumor necrosis factor in flavone acetic acid-induced tumor vasculature shutdown.

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Flavone acetic acid (FAA), a novel investigational antitumor agent, has been shown to cause early vascular shutdown in several experimental murine tumors, and this phenomenon is believed to be crucial to FAA's antitumor effects. However, the basis of this FAA-induced tumor vascular shutdown is

Flavones mitigate tumor necrosis factor-alpha-induced adhesion molecule upregulation in cultured human endothelial cells: role of nuclear factor-kappa B.

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Flavones have been classified as anti-atherogenic agents that inhibit monocyte adhesion to stimulated endothelium, possibly by blocking induction of cell adhesion molecules (CAM). This anti-atherogenic feature of these flavonoids appears to be related to their chemical structures. Flavones may

Necrosis in non-tumour tissues caused by flavone acetic acid and 5,6-dimethyl xanthenone acetic acid.

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