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Página 1 desde 132 resultados
Tumor necrosis factor-α-induced colitis increases NADPH oxidase 1 expression, oxidative stress, and neutrophil recruitment in the colon: preventive effect of apocynin.
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Reactive oxygen species- (ROS-) mediated injury has been implicated in several inflammatory disorders, including inflammatory bowel disease (IBD). NADPH oxidases (NOXs) are the major source of endogenous ROS. Here, we investigated the role of NOXs derived-ROS in a mouse model of colitis induced by
Differential upregulation of Nox homologues of NADPH oxidase by tumor necrosis factor-alpha in human aortic smooth muscle and embryonic kidney cells.
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NADPH oxidases are important sources of vascular superoxide, which has been linked to the pathogenesis of atherosclerosis. Previously we demonstrated that the Nox4 subunit of NADPH oxidase is a critical catalytic component for superoxide production in quiescent vascular smooth muscle cells. In this
Treatment with NADPH oxidase inhibitor apocynin alleviates diabetic neuropathic pain in rats.
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Increased reactive oxygen species by the activation of NADPH oxidase (NOX) contributes to the development of diabetic complications. Apocynin, a NOX inhibitor, increases sciatic nerve conductance and blood flow in diabetic rats. We investigated potential protective effect of apocynin in rat diabetic
Apocynin, a plant-derived, cartilage-saving drug, might be useful in the treatment of rheumatoid arthritis.
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OBJECTIVE
To investigate whether apocynin, 1-(4-hydroxy-3-methoxyphenyl)ethanone, is able to diminish inflammation-induced cartilage destruction in rheumatoid arthritis (RA), studied in a human in vitro model.
METHODS
Apocynin was added to cultures of RA peripheral blood mononuclear cells (PBMNC).
Tumor necrosis factor-alpha: a possible priming agent for the polymorphonuclear leukocyte-reduced nicotinamide-adenine dinucleotide phosphate oxidase in hypertension.
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In the Sabra rat, oxidative stress (OS) and inflammation precede the development of hypertension. Inhibition of the phagocytic NADPH oxidase attenuates the rise in blood pressure. The present study was set to identify possible priming agents for this enzyme and to test the hypothesis that the
Superoxide production and NADPH oxidase expression in human rheumatoid synovial cells: regulation by interleukin-1beta and tumour necrosis factor-alpha.
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OBJECTIVE
to evaluate the rheumatoid synovial cell capacity to produce superoxide anion in response to interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha), and to study the NADPH oxidase involvement in this production.
METHODS
Synovial cells obtained from 7 rheumatoid arthritis
Apocynin improves insulin resistance through suppressing inflammation in high-fat diet-induced obese mice.
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We investigated the effects of apocynin on high-fat diet- (HFD-) induced insulin resistance in C57BL/6 mice. After 12 weeks of HFD, the mice that exhibited insulin resistance then received 5 weeks of apocynin (2.4 g/L, in water). Following apocynin treatment, fasting glucose, insulin, and glucose
Apocynin attenuates ventilator-induced lung injury in an isolated and perfused rat lung model.
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BACKGROUND
Apocynin suppresses the generation of reactive oxygen species (ROS) that are implicated in ventilator-induced lung injury (VILI). We thus hypothesized that apocynin attenuates VILI.
METHODS
VILI was induced by mechanical ventilation with tidal volume (V(t)) of 15 ml/kg in isolated and
Docosahexaenoic acid prevented tumor necrosis factor alpha-induced endothelial dysfunction and senescence.
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We investigated how docosahexaenoic acid (DHA) regulated tumor necrosis factor-alpha (TNF-α)-induced senescence and dysfunction in endothelial cells (EC). We used RT-PCR to examine the expression of several genes related to senescence and dysfunction in EC. TNF-α-induced p21 protein levels were
Redox-sensitive regulation of macrophage-inducible nitric oxide synthase expression in vitro does not correlate with the failure of apocynin to prevent lung inflammation induced by endotoxin.
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Reactive oxygen and nitrogen species are among the crucial mediators in the development of the pathological inflammatory process in the lungs and contribute to the damage of lung epithelium. The aim of the present study was to evaluate the potential of selected antioxidants or inhibitors of NADPH
Protective effect of apocynin, a NADPH-oxidase inhibitor, against contrast-induced nephropathy in the diabetic rats: a comparison with n-acetylcysteine.
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The aim of this study was to investigate the effects of apocynin, a NADPH (nicotinamide adenine dinucleotide phosphate)-oxidase inhibitor, in diabetic rats with nephropathy induced by contrast medium (CIN). Diabetes was induced in male Wistar rats by a single dose of streptozotocin (60 mg/kg i.v.).
Apocynin attenuates ischemia-reperfusion lung injury in an isolated and perfused rat lung model.
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Apocynin suppresses the generation of reactive oxygen species (ROS) that are implicated in ischemia-reperfusion (I/R) lung injury. We thus hypothesized that apocynin attenuates I/R. Furthermore, we explored the mechanisms by which apocynin may attenuate I/R. I/R was induced in an isolated and
Apocynin suppressed the nuclear factor-κB pathway and attenuated lung injury in a rat hemorrhagic shock model.
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The aim of this study was to investigate whether a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox) inhibitor, apocynin, reduces reactive oxygen species (ROS) production, suppresses the nuclear factor κB (NF-κB) pathway, attenuates lung injury, and improves survival in rat
Intracellular pathways involved in tumor necrosis factor-alpha release by human monocytes on stimulation with lipopolysaccharide or staphylococcal peptidoglycan are partly similar.
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This study compared the effects of intracellular pathway inhibitors on tumor necrosis factor-alpha (TNF-alpha) release from human monocytes. Cells were stimulated with peptidoglycan (PG) from Staphylococcus epidermidis or with Escherichia coli lipopolysaccharide (LPS), both in the presence of 10%
[Advanced oxidation protein products-induced tumor necrosis factor alpha secretion in monocytes via reactive oxygen species generation].
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OBJECTIVE
To investigate the effect of advanced oxidation protein products (AOPP) on the secretion of tumor necrosis factor alpha eTNFalphae in monocytes and its possible mechanism.
METHODS
Human monocyte cell line THP-1 and peripheral blood monocytes were incubated with AOPP-bovine serum
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