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nicotinic acid/radang
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Modulation of Intestinal Barrier and Bacterial Endotoxin Production Contributes to the Beneficial Effect of Nicotinic Acid on Alcohol-Induced Endotoxemia and Hepatic Inflammation in Rats.
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Alcohol consumption causes nicotinic acid deficiency. The present study was undertaken to determine whether dietary nicotinic acid supplementation provides beneficial effects on alcohol-induced endotoxin signaling and the possible mechanisms at the gut-liver axis. Male Sprague-Dawley rats were
Action of nicotinic acid on the reversion of hypoxic-inflammatory link on 3T3-L1 adipocytes.
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BACKGROUND
Hypoxia resulting from adipocyte expansion is considered the basis of the inflammatory milieu observed in Metabolic Syndrome. Nicotinic acid can act on adipocytes interfering on the inflammatory response. In this study, we investigated the role of HIF-1 α (hypoxia-inducible factor -1
Inflammatory degeneration of joint tissue in adjuvant arthritis after intraarticular treatment with the mixture of silver drug and nicotinic acid.
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Combination intraarticular administration of Poviargol (0.5 mg/kg) and nicotinic acid (1.0 mg/kg) reduced symptoms of local and general inflammation in rats with adjuvant arthritis. We revealed a decrease in morphological signs of inflammatory degeneration of joint tissue and reduction of metabolic
Nicotinic acid inhibits vascular inflammation via the SIRT1-dependent signaling pathway.
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Nicotinic acid (NA) has recently been shown to inhibit inflammatory response in cardiovascular disease. Sirtuin1 (SIRT1), a NAD(+)-dependent class III histone deacetylase, participates in the regulation of cellular inflammation. We hypothesized that dietary supplementation of NA could attenuate
Nicotinic acid induces antinociceptive and anti-inflammatory effects in different experimental models.
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Although in vitro studies have shown that nicotinic acid inhibits some aspects of the inflammatory response, a reduced number of in vivo studies have investigated this activity. To the best of our knowledge, the effects induced by nicotinic acid in models of nociceptive and inflammatory pain are not
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
Correction: Silk based scaffolds with immunomodulatory capacity: anti-inflammatory effects of nicotinic acid.
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Correction for 'Silk based scaffolds with immunomodulatory capacity: anti-inflammatory effects of nicotinic acid' by Abdollah Zakeri Siavashani et al., Biomater. Sci., 2019, DOI: 10.1039/c9bm00814d.
Nicotinic acid conjugates of nonsteroidal anti-inflammatory drugs (NSAID's) and their anti-inflammatory properties.
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A series of nicotinic acid conjugates with non-steroidal anti-inflammatory drugs (NSAID's) have been effectively synthesized using TBTU in high yield and purity. All the synthesized conjugates were evaluated for their in vitro anti-inflammatory activity.
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
Anti-inflammatory effects of nicotinic acid in human monocytes are mediated by GPR109A dependent mechanisms.
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OBJECTIVE
Nicotinic acid (NA) treatment has been associated with benefits in atherosclerosis that are usually attributed to effects on plasma lipoproteins. The NA receptor GPR109A is expressed in monocytes and macrophages, suggesting a possible additional role for NA in modulating function of these
Silk based scaffolds with immunomodulatory capacity: anti-inflammatory effects of nicotinic acid.
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Implantation of temporary and permanent biomaterials in the body leads to a foreign body reaction (FBR), which may adversely affect tissue repair processes and functional integration of the biomaterial. However, modulation of the inflammatory response towards biomaterials can potentially enable a
Anti-inflammatory effects of nicotinic acid in adipocytes demonstrated by suppression of fractalkine, RANTES, and MCP-1 and upregulation of adiponectin.
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OBJECTIVE
A major site of action for the atheroprotective drug nicotinic acid (NA) is adipose tissue, via the G-protein-coupled receptor, GPR109A. Since, adipose tissue is an active secretory organ that contributes both positively and negatively to systemic inflammatory processes associated with
Anti-inflammatory and Anti-nociceptive Activity of Ruthenium Complexes with Isonicotinic and Nicotinic Acids (Niacin) as Ligands.
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This work evaluated the analgesic and anti-inflammatory activity of ruthenium(II) complexes trans-[Ru(NO(+))(NH3)4(L)](BF4)3 and [Ru(NH3)5(L)](BF4)3 containing the nonsteroidal anti-inflammatory drugs nicotinic acid (Hnic) and its isomer isonicotinic acid (ina) as ligands (L). The anti-nociceptive
Nicotinic Acid Receptor GPR109A Exerts Anti-Inflammatory Effects Through Inhibiting the Akt/mTOR Signaling Pathway in MIN6 Pancreatic β cells.
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OBJECTIVE
We found that activation of the nicotinic acid receptor GPR109A, expressed by the MIN6 murine pancreatic β cell line, inhibits nitric oxide accumulation induced by IFN-γ and TNF-α, implicating an anti-inflammatory effect of GPR109A in MIN6 cells. Nevertheless, the mechanism of its
[Hepato-gastroenteric inflammatory syndrome treated intraduodenally with oxymethyl amide of nicotinic acid].
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