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mevalonic acid/infiammazione
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Pagina 1 a partire dal 58 risultati
A new HMG-CoA reductase inhibitor, rosuvastatin, exerts anti-inflammatory effects on the microvascular endothelium: the role of mevalonic acid.
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Recent studies have reported that hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors have vasculoprotective effects independent of their lipid-lowering properties, including anti-inflammatory actions. We used intravital microscopy of the rat mesenteric microvasculature to examine the
Statins inhibit A beta-neurotoxicity in vitro and A beta-induced vasoconstriction and inflammation in rat aortae.
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Freshly solubilized A beta peptides synergistically increase the magnitude of the constriction induced by endothelin-1 (ET-1), via the activation of a pro-inflammatory pathway. We report that mevinolin and mevastatin, two inhibitors of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase
Statins and inflammation: an update.
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OBJECTIVE
Randomized trials have suggested that the beneficial effects of statins could extend to mechanisms beyond cholesterol reduction. Investigations have shown that statins are associated with reduced plasma markers of inflammation, reduced T-cell and monocyte activation, and reduced blood
Inhibition of protein prenylation down-regulates signalling by inflammatory mediators in human keratinocytes.
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Several inflammatory mediators have been shown to activate phospholipase C in human keratinocytes via GTP-binding protein-coupled receptors. Since GTP-binding proteins are prenylated proteins, we have examined the role of prenylation in signal transduction in HaCaT keratinocytes. Indirect inhibition
Fluvastatin attenuates IGF-1-induced ERK1/2 activation and cell proliferation by mevalonic acid depletion in human mesangial cells.
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OBJECTIVE
Insulin-like growth factor (IGF)-1 is a major mitogenic growth factor for mesangial cells (MCs). Statins slow the progression of chronic kidney disease by affecting inflammatory cell signaling pathways, in addition to improving lipid profile, however, no studies have investigated the
Prolonged treatment with mevalonolactone induces oxidative stress response with reactive oxygen species production, mitochondrial depolarization and inflammation in human glioblastoma U-87 MG cells.
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Mevalonate pathway impairment has been observed in diverse diseases, including Mevalonate Kinase Deficiency (MKD). MKD is a hereditary auto-inflammatory disorder, due to mutations at mevalonate kinase gene (MVK), encoding mevalonate kinase (MK) enzyme. To date, the most accredited MKD pathogenic
[Auto-inflammatory disease with hyperimmunoglobulinemia D of late onset].
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BACKGROUND
The term "auto-inflammatory diseases" encompasses a group of disorders characterised by febrile episodes of sudden onset associated with joint, abdominal, lymph node and cutaneous signs, each presenting a genetic and/or laboratory specificity allowing their identification. Polyclonal
3-Hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors attenuate beta-amyloid-induced microglial inflammatory responses.
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Alzheimer's disease (AD) is characterized by extracellular deposits of fibrillar beta-amyloid (Abeta) in the brain, a fulminant microglial-mediated inflammatory reaction, and neuronal death. The use of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins) is associated with a reduced
When neonatal inflammation does not mean infection: an early-onset mevalonate kinase deficiency with interstitial lung disease.
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Systemic inflammation in neonates is attributable to an infection in almost all cases. When inflammation persists, an autoinflammatory disease should be promptly suspected. We report here a case of mevalonate kinase deficiency (MKD) that presented at birth with mild symptoms and signs suggestive for
A role for hydroxy-methylglutaryl coenzyme a reductase in pulmonary inflammation and host defense.
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BACKGROUND
A growing literature indicates that hydroxy-methylglutaryl coenzyme A reductase inhibitors (statins) modulate proinflammatory cellular signaling and functions. No studies to date, however, have addressed whether statins modulate pulmonary inflammation triggered by aerogenic stimuli or
Anti-inflammatory fusicoccane-type diterpenoids from the phytopathogenic fungus Alternaria brassicicola.
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Altering the cultivation conditions, such as temperature, media compositions, illumination, aeration, the shape of the culturing flask, etc., is regarded as a useful strategy for the exploitation of structurally novel and bioactive secondary metabolites, which inspired us to explore the chemical and
Anti-inflammatory effect of pitavastatin on NF-kappaB activated by TNF-alpha in hepatocellular carcinoma cells.
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As nuclear factor-kappa B (NF-kappaB) is essential for promoting inflammation-associated cancer, it is a potential target for cancer prevention in chronic inflammatory diseases. Here we examined the anti-inflammatory effect of pitavastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase
Simvastatin treatment for inflammatory attacks of the hyperimmunoglobulinemia D and periodic fever syndrome.
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Hyperimmunoglobulinemia D (hyper-IgD) and periodic fever syndrome, a hereditary autoinflammatory syndrome, is characterized by lifelong recurrent episodes of fever and inflammation. No effective treatment is known. It is caused by a defect of mevalonate kinase, an enzyme that follows
Induction of scavenger receptor class B type I is critical for simvastatin enhancement of high-density lipoprotein-induced anti-inflammatory actions in endothelial cells.
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Changes in plasma lipoprotein profiles, especially low levels of high-density lipoprotein (HDL), are a common biomarker for several inflammatory and immune diseases, including atherosclerosis and rheumatoid arthritis. We examined the effect of simvastatin on HDL-induced anti-inflammatory actions.
Induction of apoptosis and inhibition of migration of inflammatory and vascular wall cells by cerivastatin.
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Statins are thought to play a role in directly affecting immune and mesenchymal cells. Since cerivastatin's pleiotropic effects are poorly investigated, we were interested to find out whether this drug can modulate leukocyte and vessel wall cell functions. Leukocyte migration was tested in modified
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