mevalonic acid/necrosis

Lyen an sove nan clipboard la

AtikEsè klinikPatant

Chwazi kalite sòt

Paj 1 soti nan 19 rezilta yo

Statins increase thrombomodulin expression and function in human endothelial cells by a nitric oxide-dependent mechanism and counteract tumor necrosis factor alpha-induced thrombomodulin downregulation.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Expression of functionally active thrombomodulin (TM) on the luminal surface of endothelial cells is critical for vascular thromboresistance. TM maintains thrombohemorrhagic homeostasis by forming a complex with thrombin, which subsequently loses its procoagulant properties and instead activates

Simvastatin inducing PC3 prostate cancer cell necrosis mediated by calcineurin and mitochondrial dysfunction.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

In the present study we analyzed the mechanisms of simvastatin toxicity for the PC3 human prostate cancer cell line. At 10 microM, simvastatin induced principally apoptosis, which was prevented by mevalonic acid but not by cyclosporin A, the inhibitor of calcineurin and mitochondrial permeability

Simvastatin inhibits production of interleukin 6 (IL-6) and IL-8 and cell proliferation induced by tumor necrosis factor-alpha in fibroblast-like synoviocytes from patients with rheumatoid arthritis.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

OBJECTIVE Rheumatoid arthritis (RA) is a chronic inflammatory disease in which the synovial environment is characterized by intense immunological activity. Evidence suggests that statins modulate immune functions and may have a beneficial effect on patients with RA. We investigated whether

Tumor necrosis factor-alpha-induced production of plasminogen activator inhibitor 1 and its regulation by pioglitazone and cerivastatin in a nonmalignant human hepatocyte cell line.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Plasminogen activator inhibitor 1 (PAI-1) is an important mediator of atherosclerosis and liver fibrosis in insulin resistance. Circulating levels of PAI-1 are elevated in obese individuals, and PAI-1 messenger RNA is significantly higher in the livers of obese type 2 diabetic individuals than in

Zoledronic acid prevents the hepatic changes associated with high fat diet in rats; the potential role of mevalonic acid pathway in nonalcoholic steatohepatitis.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

The role of hepatic free cholesterol (FC) in nonalcoholic steatohepatitis (NASH) is raised up and the intervention with cholesterol synthesis will be a potential therapeutic target. This study investigated the hepatoprotective effect of mevalonic acid pathway inhibition by Zoledronic acid (ZA) on

Perinatal manifestation of mevalonate kinase deficiency and efficacy of anakinra.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

BACKGROUND Mevalonate kinase deficiency is a metabolic autoinflammatory syndrome caused by mutations in the MVK gene, mevalonate kinase, the key enzyme in the non-sterol isoprenoid biosynthesis pathway. Two phenotypes of mevalonate kinase deficiency are known based on the level of enzymatic

Mevalonate-dependent inhibition of transendothelial migration and chemotaxis of human peripheral blood neutrophils by pravastatin.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Pravastatin, a hydrophilic inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, has been reported to beneficially affect atherogenesis, plaque stability, and transient myocardial ischemia in significant coronary artery disease by influencing lipid metabolism and by intracellular signaling

Statin-induced apoptosis of vascular endothelial cells is blocked by dexamethasone.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Statins block de novo synthesis of cholesterol by inhibiting the enzyme, HMG CoA reductase. The product of this reaction, mevalonic acid, is also a precursor of isoprenoids, molecules required for the activation of signalling G-proteins, such as Ras. Signal transduction pathways involving Ras are

3-hydroxy-3-methylglutaryl coenzyme A reductase-independent inhibition of CD40 expression by atorvastatin in human endothelial cells.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

OBJECTIVE 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) exert potent anti-inflammatory effects that are independent of their cholesterol-lowering action. We have investigated the effects of these drugs on cytokine-stimulated CD40 expression in human cultured

Molecular analysis of the MVK and TNFRSF1A genes in patients with a clinical presentation typical of the hyperimmunoglobulinemia D with periodic fever syndrome: a low-penetrance TNFRSF1A variant in a heterozygous MVK carrier possibly influences the phenotype of hyperimmunoglobulinemia D with periodic fever syndrome or vice versa.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

OBJECTIVE To describe biochemical findings and the spectrum of mevalonate kinase (MVK) gene mutations as well as an associated TNFRSF1A low-penetrance variant in a series of patients with clinical features of the hyperimmunoglobulinemia D with periodic fever syndrome (HIDS). METHODS The MVK gene was

Selective inhibition of formyl-methionyl-leucyl-phenylalanine (fMLF)-dependent superoxide generation in neutrophils by pravastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

It has been shown previously that inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, such as compactin, lovastatin, and pravastatin, block cholesterol synthesis, suppress lymphocyte functions, and beneficially affect atherogenesis. Recently, it was reported that compactin and

Statins decrease TNF-alpha-induced osteoprotegerin production by endothelial cells and smooth muscle cells in vitro.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Recent reports have implicated osteoprotegerin (OPG) in cardiovascular disease processes. Endothelial and smooth muscle cells produce OPG and its expression in these cells is upregulated by inflammatory mediators. Statins, which besides their lipid lowering properties have various vasculoprotective

Zoledronic acid inhibits RANK expression and migration of osteoclast precursors during osteoclastogenesis.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Bisphosphonates have been known to directly inhibit bone resorption and promote apoptosis in mature osteoclasts. Although bisphosphonates have been recognized as the most effective drugs to treat osteoporosis and bone cancer metastasis, the exact effects and mechanism(s) of bisphosphonates on

Extracellular signal-regulated kinase inhibition by statins inhibits neutrophil activation by ANCA.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

BACKGROUND 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) may modulate cellular inflammatory functions independent of serum cholesterol. We tested the hypothesis that statins decrease respiratory burst activity of human polymorphonuclear neutrophils (PMN) in response

High concentration simvastatin induces apoptosis in fibroblast-like synoviocytes from patients with rheumatoid arthritis.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

OBJECTIVE We previously reported that 10 mg/day of simvastatin significantly reduced clinical scores of rheumatoid arthritis (RA) in patients with active RA with hypercholesterolemia. We have also reported that a certain pharmacological concentration of simvastatin, i.e., 0.05-0.1 microM, inhibits

Antre nan paj
facebook nou an

Herbal & Natural Medicine

Baz done ki pi konplè remèd fèy medsin te apiye nan syans

Travay nan 55 lang
Geri èrbal te apiye nan syans
Remèd fèy rekonesans pa imaj
Kat entèaktif GPS - tag zèb sou kote (vini byento)
Li piblikasyon syantifik ki gen rapò ak rechèch ou an
Search remèd fèy medsin pa efè yo
Izeganize enterè ou yo ak rete kanpe fè dat ak rechèch la nouvèl, esè klinik ak rive

Tape yon sentòm oswa yon maladi epi li sou remèd fèy ki ta ka ede, tape yon zèb ak wè maladi ak sentòm li itilize kont.
* Tout enfòmasyon baze sou rechèch syantifik pibliye