Avicularin Inhibits Lipopolysaccharide-Induced Inflammatory Response by Suppressing ERK Phosphorylation in RAW 264.7 Macrophages
suppresAvicularin, quercetin-3-α-L-arabinofuranoside, has been reported to possess diverse pharmacological properties such as anti-inflammatory and anti-infectious effects. However, the underlying mechanism by which avicularin exerts its anti-inflammatory activity has not been clearly demonstrated....
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The Korean Society of Applied Pharmacology
2012
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Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3762284/ |
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pubmed-37622842013-09-05 Avicularin Inhibits Lipopolysaccharide-Induced Inflammatory Response by Suppressing ERK Phosphorylation in RAW 264.7 Macrophages Vo, Van Anh Lee, Jae-Won Chang, Ji-Eun Kim, Ji-Young Kim, Nam-Ho Lee, Hee Jae Kim, Sung-Soo Chun, Wanjoo Kwon, Yong-Soo Articles suppresAvicularin, quercetin-3-α-L-arabinofuranoside, has been reported to possess diverse pharmacological properties such as anti-inflammatory and anti-infectious effects. However, the underlying mechanism by which avicularin exerts its anti-inflammatory activity has not been clearly demonstrated. This study aimed to elucidate the anti-inflammatory mechanism of avicularin in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. Avicularin significantly inhibited LPS-induced excessive production of pro-inflammatory mediators such as nitric oxide (NO) and PGE2 and the protein levels of iNOS and COX-2, which are responsible for the production of NO and PGE2, respectively. Avicularin also suppressed LPS-induced overproduction of pro-inflammatory cytokine IL-1β. Furthermore, avicularin significantly suppressed LPS-induced degradation of IκB, which retains NF-κB in the cytoplasm, consequently inhibiting the transcription of pro-inflammatory genes by NF-κB in the nucleus. To understand the underlying signaling mechanism of anti-inflammatory activity of avicularin, involvement of multiple kinases was examined. Avicularin significantly attenuated LPS-induced activation of ERK signaling pathway in a concentration-dependent manner. Taken together, the present study clearly demonstrates that avicularin exhibits anti-inflammatory activity through the suppression of ERK signaling pathway in LPS-stimulated RAW 264.7 macrophage cells. The Korean Society of Applied Pharmacology 2012-11 /pmc/articles/PMC3762284/ /pubmed/24009846 http://dx.doi.org/10.4062/biomolther.2012.20.6.532 Text en Copyright ©2012, The Korean Society of Pharmaceutics |
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Open Access Journal |
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Foreign Institution |
institution |
US National Center for Biotechnology Information |
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NCBI PubMed |
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Online Access |
language |
English |
format |
Online |
author |
Vo, Van Anh Lee, Jae-Won Chang, Ji-Eun Kim, Ji-Young Kim, Nam-Ho Lee, Hee Jae Kim, Sung-Soo Chun, Wanjoo Kwon, Yong-Soo |
spellingShingle |
Vo, Van Anh Lee, Jae-Won Chang, Ji-Eun Kim, Ji-Young Kim, Nam-Ho Lee, Hee Jae Kim, Sung-Soo Chun, Wanjoo Kwon, Yong-Soo Avicularin Inhibits Lipopolysaccharide-Induced Inflammatory Response by Suppressing ERK Phosphorylation in RAW 264.7 Macrophages |
author_facet |
Vo, Van Anh Lee, Jae-Won Chang, Ji-Eun Kim, Ji-Young Kim, Nam-Ho Lee, Hee Jae Kim, Sung-Soo Chun, Wanjoo Kwon, Yong-Soo |
author_sort |
Vo, Van Anh |
title |
Avicularin Inhibits Lipopolysaccharide-Induced Inflammatory Response by Suppressing ERK Phosphorylation in RAW 264.7 Macrophages |
title_short |
Avicularin Inhibits Lipopolysaccharide-Induced Inflammatory Response by Suppressing ERK Phosphorylation in RAW 264.7 Macrophages |
title_full |
Avicularin Inhibits Lipopolysaccharide-Induced Inflammatory Response by Suppressing ERK Phosphorylation in RAW 264.7 Macrophages |
title_fullStr |
Avicularin Inhibits Lipopolysaccharide-Induced Inflammatory Response by Suppressing ERK Phosphorylation in RAW 264.7 Macrophages |
title_full_unstemmed |
Avicularin Inhibits Lipopolysaccharide-Induced Inflammatory Response by Suppressing ERK Phosphorylation in RAW 264.7 Macrophages |
title_sort |
avicularin inhibits lipopolysaccharide-induced inflammatory response by suppressing erk phosphorylation in raw 264.7 macrophages |
description |
suppresAvicularin, quercetin-3-α-L-arabinofuranoside, has been reported to possess diverse pharmacological properties such as anti-inflammatory and anti-infectious effects. However, the underlying mechanism by which avicularin exerts its anti-inflammatory activity has not been clearly demonstrated. This study aimed to elucidate the anti-inflammatory mechanism of avicularin in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. Avicularin significantly inhibited LPS-induced excessive production of pro-inflammatory mediators such as nitric oxide (NO) and PGE2 and the protein levels of iNOS and COX-2, which are responsible for the production of NO and PGE2, respectively. Avicularin also suppressed LPS-induced overproduction of pro-inflammatory cytokine IL-1β. Furthermore, avicularin significantly suppressed LPS-induced degradation of IκB, which retains NF-κB in the cytoplasm, consequently inhibiting the transcription of pro-inflammatory genes by NF-κB in the nucleus. To understand the underlying signaling mechanism of anti-inflammatory activity of avicularin, involvement of multiple kinases was examined. Avicularin significantly attenuated LPS-induced activation of ERK signaling pathway in a concentration-dependent manner. Taken together, the present study clearly demonstrates that avicularin exhibits anti-inflammatory activity through the suppression of ERK signaling pathway in LPS-stimulated RAW 264.7 macrophage cells. |
publisher |
The Korean Society of Applied Pharmacology |
publishDate |
2012 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3762284/ |
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1612008181514371072 |