skip to main content
OSTI.GOV title logo U.S. Department of Energy
Office of Scientific and Technical Information

Title: Anti-inflammatory and antifibrotic effects of methyl palmitate

Abstract

Methyl palmitate (MP) has been shown earlier to inhibit Kupffer cells and rat peritoneal macrophages. To evaluate the potential of MP to inhibit the activation of other macrophages, RAW cells (macrophages of alveolar origin) were treated with varying concentrations of MP (0.25, 0.5, 1 mM). Assessment of cytotoxicity using MTT assay revealed that 0.25 and 0.5 mM are not toxic to RAW cells. MP was able to inhibit the phagocytic function of RAW cells. Treatment of cells with MP 24 hours prior to LPS stimulation significantly decreased nitric oxide release and altered the pattern of cytokines release; there was a significant decrease in TNF-{alpha} and a significant increase in IL-10 compared to the controls. However, there is a non-significant change in IL-6 level. Furthermore, phosphorylation of inhibitory kappa B (I{kappa}B{alpha}) protein was significantly decreased in RAW cells treated with 0.5 mM MP after LPS stimulation. Based upon the in-vitro results, it was examined whether MP treatment will be effective in preventing bleomycin-induced lung inflammation and fibrosis in-vivo. Bleomycin given by itself caused destruction of the lung architecture characterized by pulmonary fibrosis with collapse of air alveoli and emphysematous. Bleomycin induced a significant increase in hydroxyproline level and activated NF-{kappa}B, p65more » expression in the lung. MP co-treatment significantly ameliorated bleomycin effects. These results suggest that MP has a potential of inhibiting macrophages in general. The present study demonstrated for the first time that MP has anti-inflammatory and antifibrotic effect that could be through NF-kB inhibition. Thus MP like molecule could be a promising anti-inflammatory and antifibrotic drug. - Research Highlights: >Methyl palmitate is a universal macrophage inhibitor. >It could be a promising nucleus of anti-inflammatory and antifibrotic drugs. >The underlying mechanism of these effects could be through NF-kB inhibition.« less

Authors:
Publication Date:
OSTI Identifier:
21587805
Resource Type:
Journal Article
Journal Name:
Toxicology and Applied Pharmacology
Additional Journal Information:
Journal Volume: 254; Journal Issue: 3; Other Information: DOI: 10.1016/j.taap.2011.04.016; PII: S0041-008X(11)00155-4; Copyright (c) 2011 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0041-008X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; BLEOMYCIN; FIBROSIS; HYDROXYPROLINE; IN VITRO; IN VIVO; INFLAMMATION; INHIBITION; LUNGS; LYMPHOKINES; MACROPHAGES; NITRIC OXIDE; PHOSPHORYLATION; RATS; RETICULOENDOTHELIAL SYSTEM; STIMULATION; TOXICITY; AMINES; AMINO ACIDS; ANIMAL CELLS; ANIMAL TISSUES; ANIMALS; ANTIBIOTICS; ANTI-INFECTIVE AGENTS; ANTIMITOTIC DRUGS; ANTINEOPLASTIC DRUGS; AZOLES; BODY; CARBOXYLIC ACIDS; CHALCOGENIDES; CHEMICAL REACTIONS; CONNECTIVE TISSUE CELLS; DRUGS; GROWTH FACTORS; HETEROCYCLIC ACIDS; HETEROCYCLIC COMPOUNDS; HYDROXY ACIDS; MAMMALS; MITOGENS; NITROGEN COMPOUNDS; NITROGEN OXIDES; ORGANIC ACIDS; ORGANIC COMPOUNDS; ORGANIC NITROGEN COMPOUNDS; ORGANS; OXIDES; OXYGEN COMPOUNDS; PATHOLOGICAL CHANGES; PHAGOCYTES; PROTEINS; PYRROLES; PYRROLIDINES; RESPIRATORY SYSTEM; RODENTS; SOMATIC CELLS; SYMPTOMS; VERTEBRATES

Citation Formats

El-Demerdash, Ebtehal, E-mail: ebtehal_dm@yahoo.com. Anti-inflammatory and antifibrotic effects of methyl palmitate. United States: N. p., 2011. Web. doi:10.1016/j.taap.2011.04.016.
El-Demerdash, Ebtehal, E-mail: ebtehal_dm@yahoo.com. Anti-inflammatory and antifibrotic effects of methyl palmitate. United States. doi:10.1016/j.taap.2011.04.016.
El-Demerdash, Ebtehal, E-mail: ebtehal_dm@yahoo.com. Mon . "Anti-inflammatory and antifibrotic effects of methyl palmitate". United States. doi:10.1016/j.taap.2011.04.016.
@article{osti_21587805,
title = {Anti-inflammatory and antifibrotic effects of methyl palmitate},
author = {El-Demerdash, Ebtehal, E-mail: ebtehal_dm@yahoo.com},
abstractNote = {Methyl palmitate (MP) has been shown earlier to inhibit Kupffer cells and rat peritoneal macrophages. To evaluate the potential of MP to inhibit the activation of other macrophages, RAW cells (macrophages of alveolar origin) were treated with varying concentrations of MP (0.25, 0.5, 1 mM). Assessment of cytotoxicity using MTT assay revealed that 0.25 and 0.5 mM are not toxic to RAW cells. MP was able to inhibit the phagocytic function of RAW cells. Treatment of cells with MP 24 hours prior to LPS stimulation significantly decreased nitric oxide release and altered the pattern of cytokines release; there was a significant decrease in TNF-{alpha} and a significant increase in IL-10 compared to the controls. However, there is a non-significant change in IL-6 level. Furthermore, phosphorylation of inhibitory kappa B (I{kappa}B{alpha}) protein was significantly decreased in RAW cells treated with 0.5 mM MP after LPS stimulation. Based upon the in-vitro results, it was examined whether MP treatment will be effective in preventing bleomycin-induced lung inflammation and fibrosis in-vivo. Bleomycin given by itself caused destruction of the lung architecture characterized by pulmonary fibrosis with collapse of air alveoli and emphysematous. Bleomycin induced a significant increase in hydroxyproline level and activated NF-{kappa}B, p65 expression in the lung. MP co-treatment significantly ameliorated bleomycin effects. These results suggest that MP has a potential of inhibiting macrophages in general. The present study demonstrated for the first time that MP has anti-inflammatory and antifibrotic effect that could be through NF-kB inhibition. Thus MP like molecule could be a promising anti-inflammatory and antifibrotic drug. - Research Highlights: >Methyl palmitate is a universal macrophage inhibitor. >It could be a promising nucleus of anti-inflammatory and antifibrotic drugs. >The underlying mechanism of these effects could be through NF-kB inhibition.},
doi = {10.1016/j.taap.2011.04.016},
journal = {Toxicology and Applied Pharmacology},
issn = {0041-008X},
number = 3,
volume = 254,
place = {United States},
year = {2011},
month = {8}
}