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Rat Peritoneal Macrophages (rat + peritoneal_macrophage)
Selected AbstractsMethyl palmitate inhibits lipopolysaccharide-stimulated phagocytic activity of rat peritoneal macrophagesJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 6 2006Swapna Sarkar Abstract Macrophages, in general, are critical effectors of body's immune system. Chemical inhibition of phagocytic activity of such macrophages as Kupffer cells has been extensively studied. We have earlier shown that methyl palmitate (MP) inhibits the activation of Kupffer cells. To evaluate the potential of MP to inhibit the activation of other macrophages, we treated rat peritoneal macrophages with varying concentrations of MP. Its treatment led to a dose-dependent inhibition of phagocytic activity, which was found to be 34%, 47%, and 66% at 0.25, 0.50, and 1.0 mM MP, respectively, as measured by latex bead uptake. When MP-treated peritoneal macrophages were stimulated with lipopolysaccharide (LPS), the nitric oxide (.NO) release was inhibited at 6 h, while cyclooxygenase-2 expression decreased after 24 h. The treatment with MP increased the release of interleukin (IL)-10 in the LPS-treated cells at 6 h, while IL-6 and tumor necrosis factor-, were significantly increased both at 6 and 24 h. Our data suggest that MP inhibits phagocytic activity and . NO production similar to that observed in isolated Kupffer cells. Therefore, inhibition of phagocytosis by MP may be a general phenomenon, and it could be used as an inhibitor of macrophage function. © 2006 Wiley Periodicals, Inc. J Biochem Mol Toxicol 20:302,308, 2006; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20150 [source] Blockade of chloride intracellular ion channel 1 stimulates A, phagocytosisJOURNAL OF NEUROSCIENCE RESEARCH, Issue 11 2008Silvia Paradisi Abstract In amyloid-, (A,)-stimulated microglial cells, blockade of chloride intracellular ion channel 1 (CLIC1) reverts the increase in tumor necrosis factor-, and nitric oxide (NO) production and results in neuroprotection of cocultured neurons. This effect could be of therapeutic efficacy in Alzheimer's disease (AD), where microglial activation may contribute to neurodegeneration, but it could reduce A, phagocytosis, which could facilitate amyloid plaque removal. Here, we analyzed the CLIC1 blockade effect on A,-stimulated mononuclear phagocytosis. In the microglial cell line BV-2, A,25,35 treatment enhanced fluorescent bead phagocytosis, which persisted also in the presence of IAA-94, a CLIC1 channel blocker. The same result was obtained in rat primary microglia and in BV2 cells, where CLIC1 expression had been knocked down with a plasmid producing small interfering RNAs. To address specifically the issue of A, phagocytosis, we treated BV-2 cells with biotinylated A,1,42 and measured intracellular amyloid by morphometric analysis. IAA-94-treated cells showed an increased A, phagocytosis after 24 hr and efficient degradation of ingested material after 72 hr. In addition, we tested A,1,42 phagocytosis in adult rat peritoneal macrophages. Also, these cells actively phagocytosed A,1,42 in the presence of IAA-94. However, the increased expression of inducible NO synthase (iNOS), stimulated by A,, was reverted by IAA-94. In parallel, a decrease in NO release was detected. These results suggest that blockade of CLIC1 stimulates A, phagocytosis in mononuclear phagocytes while inhibiting the induction of iNOS and further point to CLIC1 as a possible therapeutic target in AD. © 2008 Wiley-Liss, Inc. [source] Inhibition of TPA-induced NF-,B nuclear translocation and production of NO and PGE2 by the anti-rheumatic gold compoundsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 2 2003Masamichi Yamashita ABSTRACT Auranofin, aurothioglucose and aurothiomalate (10 ,M each) inhibited 12- O -tetradecanoylphorbol 13-acetate (TPA, 16.2 nM)-induced nuclear translocation of nuclear factor-kappa B (NF-,B), and production of nitric oxide (NO) and prostaglandin E2 (PGE2) in rat peritoneal macrophages when the cells were pre-incubated with each gold compound for 20h. Without pre-incubation for 20h, aurothioglucose and aurothiomalate, but not auranofin, failed to inhibit the TPA-induced NF-,B nuclear translocation and production of NO and PGE2. Auranofin, aurothioglucose and aurothiomalate did not affect the direct binding of NF-,B to the DNA probe. It was suggested that these gold compounds inhibit the TPA-induced production of NO and PGE2 by inhibiting the NF-,B nuclear translocation. [source] Lignans from Acanthopanax chiisanensis having an inhibitory activity on prostaglandin E2 productionPHYTOTHERAPY RESEARCH, Issue 2 2005Sanghyun Lee Abstract The chloroform and the ethyl acetate fractions from the roots of Acanthopanax chiisanensis exhibited the significant inhibition of TPA-induced prostaglandin E2 (PGE2) production in rat peritoneal macrophages. Five lignans were isolated from the chloroform fraction and their structures were elucidated as l -sesamin, helioxanthin, savinin, taiwanin C, and 3-(3,4-dimethoxybenzyl)-2-(3,4-methylenedioxybenzyl)butyrolactone. Among the lignans tested, taiwanin C showed the most potent inhibitory activity (IC50 = 0.12 µM) on PGE2 production with the relative order of potency, taiwanin C , 3-(3,4-dimethoxybenzyl)-2-(3,4-methylenedioxybenzyl)butyrolactone > savinin = helioxanthin. l -Sesamin showed no inhibitory activity at 30 µM. Copyright © 2005 John Wiley & Sons, Ltd. [source] Nimbidin suppresses functions of macrophages and neutrophils: relevance to its antiin,ammatory mechanismsPHYTOTHERAPY RESEARCH, Issue 5 2004Gurpreet Kaur Abstract Nimbidin is a mixture of tetranortriterpenes and is the major active principle of the seed oil of Azadirachta indica A. Juss (Meliaceae) possessing potent antiin,ammatory and antiarthritic activities. The present study revealed that nimbidin signi,cantly inhibited some of the functions of macrophages and neutrophils relevant to the in,ammatory response following both in vivo and in vitro exposure. Oral administration of 5,25 mg/kg nimbidin to rats for 3 consecutive days signi,cantly inhibited the migration of macrophages to their peritoneal cavities in response to in,ammatory stimuli and also inhibited phagocytosis and phorbol-12-myristate-13-acetate (PMA) stimulated respiratory burst in these cells. In vitro exposure of rat peritoneal macrophages to nimbidin also inhibited phagocytosis and PMA stimulated respiratory burst in these cells. Nimbidin also inhibited nitric oxide (NO) and prostaglandin E2 (PGE2) production in lipopolysaccharide (LPS) stimulated macrophages following in vitro exposure, whereas interleukin 1 (IL-1) was only weakly inhibited. Probing the mechanism of NO inhibition revealed that nimbidin ameliorated the induction of inducible NO synthase (iNOS) without any inhibition in its catalytic activity. In addition, nimbidin also attenuated degranulation in neutrophils assessed in terms of release of , -glucuronidase, myeloperoxidase and lysozyme. The results suggest that nimbidin suppresses the functions of macrophages and neutrophils relevant to in,ammation. Thus nimbidin can be valuable in treating in,ammation/in,ammatory diseases. Copyright © 2004 John Wiley & Sons, Ltd. [source] | ||||||||||