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nicotinic acid/некроза
Линкът е запазен в клипборда
Страница 1 от 27 резултата
Pyrimidinyl nicotinic acid and cerebrocortical necrosis.
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Identification of novel formyl peptide receptor-like 1 agonists that induce macrophage tumor necrosis factor alpha production.
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Development of immunomodulatory agents that enhance innate immune responses represents a promising strategy for combating infectious diseases. In the present studies, we screened a series of 71 arylcarboxylic acid hydrazide derivatives for their ability to induce macrophage tumor necrosis factor
Anti-diabetic effect of trigonelline and nicotinic acid, on KK-A(y) mice.
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Trigonelline (TRG) and nicotinic acid (NA), in which the former but not the latter improved the blood glucose level in the oral glucose tolerance test (OGTT) in Goto-Kakizaki (GK) rats were tested for anti-diabetic effects in mellitus models of KK-A(y) obese mice that had type 2 diabetes. Blood
Calcium signalling and pancreatic cell death: apoptosis or necrosis?
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Secretagogues, such as cholecystokinin and acetylcholine, utilise a variety of second messengers (inositol trisphosphate, cADPR and nicotinic acid adenine dinucleotide phosphate) to induce specific oscillatory patterns of calcium (Ca(2+)) signals in pancreatic acinar cells. These are tightly
Role of free fatty acids in catecholamine-induced cardiac necrosis.
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Previous studies have demonstrated that catecholamines produce massiive disseminated cardiac necrosis closely resembling experimental myocardial infarction. Since catecholamine-induced lipolysis increases myocardial oxygen demand and increased levels of FFA are associated with a depression of
Poly(adenosine diphosphate ribose) polymerase inhibition prevents necrosis induced by H2O2 but not apoptosis.
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OBJECTIVE
H2O2 causes DNA damage, which activates poly(adenosine diphosphate ribose) polymerase (PARP), a nuclear enzyme that uses nicotinamide adenine dinucleotide (NAD) as a substrate. When DNA strand breaks are extensive, consumption of NAD by PARP can cause adenosine triphosphate depletion. The
Improved skin flap survival with nicotinic acid and nicotinamide in rats.
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The effects of some components of the coenzyme nicotinamide adenine dinucleotide (NAD) on tissue viability were investigated in acute island skin flaps which were constructed to exceed the blood supply provided by a unilateral pedicle of inferior epigastric vessels. Control flaps undergo significant
Tumor necrosis factor alpha stimulates lipolysis in adipocytes by decreasing Gi protein concentrations.
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Prolonged treatment (12-24 h) of adipocytes with tumor necrosis factor alpha (TNFalpha) stimulates lipolysis. We have investigated the hypothesis that TNFalpha stimulates lipolysis by blocking the action of endogenous adenosine. Adipocytes were incubated for 48 h with TNFalpha, and lipolysis was
Nicotinic acid has anti-atherogenic and anti-inflammatory properties on advanced atherosclerotic lesions independent of its lipid-modifying capabilities.
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Inflammation contributes to atherosclerotic plaque initiation and progression. Recent studies suggest that nicotinic acid has anti-inflammatory effects independent of its lipid-modifying capabilities. We assessed the hypothesis that administration of nicotinic acid to older apolipoprotein E
Synthesis of new nicotinic acid derivatives and their evaluation as analgesic and anti-inflammatory agents.
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A series of 2-substituted phenyl derivatives of nicotinic acid 4a-l were synthesized and evaluated for their analgesic and anti-inflammatory activities. Compounds including 2-bromophenyl substituent, 4a, c, and d, proved to display distinctive analgesic and anti-inflammatory activities in comparison
The effect of anti-lipolytic agents on isoprenaline-induced myocardial necrosis in the rat.
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The effect of inhibiting isoprenaline-induced lipolysis on the degree of damage produced in the rat myocardium by this amine has been investigated by pre-dosing rats with the anti-lipolytic agent 5-fluoro-nicotinic acid. The degree of myocardial necrosis produced in animals given isoprenaline alone
Gene regulation of CYP4F11 in human keratinocyte HaCaT cells.
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Mechanisms regulating CYP4F genes remain under investigation, although characterization of CYP4F regulatory modalities would facilitate the discovery of new drug targets. This present study shows that all-trans- and 9-cis-retinoic acids can inhibit CYP4F11 expression in human keratinocyte-derived
Effect of NMDAR-NMNAT1/2 pathway on neuronal cell damage and cognitive impairment of sevoflurane-induced aged rats.
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Objective: The possible effect of NMDAR (N-methyl-D-aspartate receptor)-NMNAT1/2 (nicotinamide/nicotinic acid mono-nucleotide adenylyltransferase) signaling pathway on the neuronal cell damage and cognitive impairment of aged rats anesthetized by sevoflurane was explored.Methods: Adult
Antihyperlipidaemic agents. Drug interactions of clinical significance.
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The available antihyperlipidaemic drugs are generally safe and effective, and major systemic adverse effects are uncommon. However, because of their complex mechanisms of action, careful monitoring is required to identify and correct potential drug interactions. Bile acid sequestrants are the most
Currently available hypolipidaemic drugs and future therapeutic developments.
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Dyslipidaemia may be treated with a number of safe and effective pharmacological agents that target specific lipid disorders through a variety of mechanisms. The bile-acid sequestrants--cholestyramine and colestipol--primarily decrease LDL cholesterol by binding bile acids, thereby decreasing
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