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Methyl palmitate inhibits lipopolysaccharide-stimulated phagocytic activity of rat peritoneal macrophages

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 poten...

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Published in:Journal of biochemical and molecular toxicology 2006-01, Vol.20 (6), p.302-308
Main Authors: Sarkar, Swapna, Khan, M. Firoze, Kaphalia, Bhupendra S., Ansari, G. A. S.
Format: Article
Language:English
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Summary: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‐α 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
ISSN:1095-6670
1099-0461
DOI:10.1002/jbt.20150