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niacin/infiammazione
Il collegamento viene salvato negli appunti
Pagina 1 a partire dal 298 risultati
Inflammation stimulates niacin receptor (GPR109A/HCA2) expression in adipose tissue and macrophages.
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Many of the beneficial and adverse effects of niacin are mediated via a G protein receptor, G protein-coupled receptor 109A/hydroxycarboxylic acid 2 receptor (GPR109A/HCA2), which is highly expressed in adipose tissue and macrophages. Here we demonstrate that immune activation increases GPR109A/HCA2
Niacin Pretreatment Attenuates Ischemia and Reperfusion of Pancreas-induced Acute Pancreatitis and Remote Lung Injury Through Suppressing Oxidative Stress and Inflammation and Activation of SIRT1.
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BACKGROUND
Lung injury subsequent to pancreatic ischemia and reperfusion (PIR) due to shock, revascularization, and pancreas transplantation is a major clinical problem. In addition to proteases, massive production and release of reactive oxygen species (ROS) and induction of inflammatory cytokines
Anti-inflammatory effect is an important property of niacin on atherosclerosis beyond its lipid-altering effects.
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Niacin has been used for decades to lower the plasma concentrations of cholesterol, free fatty acids, and triglycerides in humans, and in addition it raises more than any other drug the levels of the protective high density lipoprotein. These effects have been used to treat dyslipidemic states.
Abatement of bleomycin-induced increases in vascular permeability, inflammatory cell infiltration, and fibrotic lesions in hamster lungs by combined treatment with taurine and niacin.
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BACKGROUND
The bleomycin (BL) hamster model of interstitial pulmonary fibrosis has been widely used to study the pathogenesis of interstitial pulmonary fibrosis and to screen potentially desirable antifibrotic agents. We have recently shown that taurine and niacin in combination, diminished
The Effects of Niacin on Inflammation in Patients with Non-ST Elevated Acute Coronary Syndrome.
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BACKGROUND
In this study, we aimed to evaluate the effects of niacin on high sensitivity C reactive protein (hs-CRP) and cholesterol levels in non-ST elevated acute coronary syndrome (NSTE-ACS) patients.
METHODS
In this prospective, open label study, 48 NSTE-ACS were randomized to niacin or control
A pilot trial to examine the effect of high-dose niacin on arterial wall inflammation using fluorodeoxyglucose positron emission tomography.
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OBJECTIVE
Although studies have reported direct inhibition of inflammatory pathways with niacin, the effect of niacin on arterial wall inflammation remains unknown. We examined the effect of niacin on arterial (18)F-fluorodeoxyglucose (FDG)-positron emission tomography (PET)/computed tomography
Evidence that niacin inhibits acute vascular inflammation and improves endothelial dysfunction independent of changes in plasma lipids.
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OBJECTIVE
To determine if niacin can confer cardiovascular benefit by inhibiting vascular inflammation and improving endothelial function independent of changes in plasma lipid and lipoprotein levels.
RESULTS
New Zealand white rabbits received normal chow or chow supplemented with 0.6% or 1.2%
Extended-Release Niacin Versus Fenofibrate in HIV-Infected Participants With Low High-Density Lipoprotein Cholesterol: Effects on Endothelial Function, Lipoproteins, and Inflammation.
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BACKGROUND
Low levels of high-density lipoprotein cholesterol (HDL-C) are common in individuals with human immunodeficiency virus (HIV) infection, persist during antiretroviral therapy (ART), and are associated with increased cardiovascular disease (CVD) risk.
METHODS
Virologically controlled
The SLIM Study: Slo-Niacin® and Atorvastatin Treatment of Lipoproteins and Inflammatory Markers in Combined Hyperlipidemia.
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BACKGROUND: The combination of niacin and statin has proven value in hyperlipidemia management and heart disease prevention. However, the efficacy of the non-prescription time-release niacin, Slo-Niacin®, is little studied alone and not at all with atorvastatin. We gave Slo-Niacin® and atorvastatin,
Prolonged niacin treatment leads to increased adipose tissue PUFA synthesis and anti-inflammatory lipid and oxylipin plasma profile.
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Prolonged niacin treatment elicits beneficial effects on the plasma lipid and lipoprotein profile that is associated with a protective CVD risk profile. Acute niacin treatment inhibits nonesterified fatty acid release from adipocytes and stimulates prostaglandin release from skin Langerhans cells,
Niacin inhibits vascular inflammation via the induction of heme oxygenase-1.
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BACKGROUND
Heme oxygenase-1 (HO-1) is a cytoprotective protein whose expression is consistently associated with therapeutic benefits in a number of pathological conditions such as atherosclerotic vascular disease and inflammation. Niacin is a pleiotropic drug that slows the progression of coronary
Niacin Suppresses Progression of Atherosclerosis by Inhibiting Vascular Inflammation and Apoptosis of Vascular Smooth Muscle Cells.
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BACKGROUND Niacin is a broad-spectrum lipid-regulating drug used for the clinical therapy of atherosclerosis; however, the mechanisms by which niacin ameliorates atherosclerosis are not clear. MATERIAL AND METHODS The effect of niacin on atherosclerosis was assessed by detection of atherosclerotic
Niacin inhibits vascular inflammation via downregulating nuclear transcription factor-κB signaling pathway.
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The study aimed to investigate the effect of niacin on vascular inflammatory lesions in vivo and in vitro as well as its lipid-regulating mechanism. In vivo study revealed that niacin downregulated the levels of inflammatory factors (IL-6 and TNF-α) in plasma, suppressed protein expression of CD68
Niacin attenuates the production of pro-inflammatory cytokines in LPS-induced mouse alveolar macrophages by HCA2 dependent mechanisms.
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Niacin has been reported to have potent anti-inflammatory effects in LPS-induced acute lung injury. However, the molecular mechanism of niacin has not been fully understood. The aim of the present study was to investigate the effects of niacin on the production of pro-inflammatory cytokines TNF-α,
Niacin attenuates lung inflammation and improves survival during sepsis by downregulating the nuclear factor-κB pathway.
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OBJECTIVE
To examine whether niacin attenuates lung inflammation and improves survival during sepsis and to determine whether the beneficial effects of niacin are associated with downregulation of the nuclear factor (NF)-κB pathway.
METHODS
Prospective laboratory study.
METHODS
University
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