Histone deacetylase inhibitor, butyrate, attenuates lipopolysaccharide-induced acute lung injury in mice
<p>Abstract</p> <p>Background</p> <p>Histone deacetylase (HDAC) inhibitors, developed as promising anti-tumor drugs, exhibit their anti-inflammatory properties due to their effects on reduction of inflammatory cytokines.</p> <p>Objective</p> <p>T...
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BMC
2010-03-01
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Series: | Respiratory Research |
Online Access: | http://respiratory-research.com/content/11/1/33 |
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author | Wang Yun-Jie Zhao Jin-Bo Tian Feng Yan Xiao-Long Wang Jian Ni Yun-Feng Jiang Tao |
author_facet | Wang Yun-Jie Zhao Jin-Bo Tian Feng Yan Xiao-Long Wang Jian Ni Yun-Feng Jiang Tao |
author_sort | Wang Yun-Jie |
collection | DOAJ |
description | <p>Abstract</p> <p>Background</p> <p>Histone deacetylase (HDAC) inhibitors, developed as promising anti-tumor drugs, exhibit their anti-inflammatory properties due to their effects on reduction of inflammatory cytokines.</p> <p>Objective</p> <p>To investigate the protective effect of butyrate, a HDAC inhibitor, on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice.</p> <p>Methods</p> <p>ALI was induced in Balb/c mice by intratracheally instillation of LPS (1 mg/kg). Before 1 hour of LPS administration, the mice received butyrate (10 mg/kg) orally. The animals in each group were sacrificed at different time point after LPS administration. Pulmonary histological changes were evaluated by hematoxylin-eosin stain and lung wet/dry weight ratios were observed. Concentrations of interleukin (IL)-1β and tumor necrosis factor (TNF)-α in bronchoalveolar lavage fluid (BALF) and concentrations of nitric oxide (NO) and myeloperoxidase (MPO) activity in lung tissue homogenates were measured by enzyme-linked immunosorbent assay (ELISA). Expression of nuclear factor (NF)-κB p65 in cytoplasm and nucleus was determined by Western blot analysis respectively.</p> <p>Results</p> <p>Pretreatment with butyrate led to significant attenuation of LPS induced evident lung histopathological changes, alveolar hemorrhage, and neutrophils infiltration with evidence of reduced MPO activity. The lung wet/dry weight ratios, as an index of lung edema, were reduced by butyrate administration. Butyrate also repressed the production of TNF-α, IL-1β and NO. Furthermore, the expression of NF-κB p65 in nucleus was markedly suppressed by butyrate pretreatment.</p> <p>Conclusions</p> <p>Butyrate had a protective effect on LPS-induced ALI, which may be related to its effect on suppression of inflammatory cytokines production and NF-κB activation.</p> |
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issn | 1465-9921 |
language | English |
last_indexed | 2024-04-14T03:39:56Z |
publishDate | 2010-03-01 |
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series | Respiratory Research |
spelling | doaj.art-d08e19f5a589445da7fed813f7d956892022-12-22T02:14:34ZengBMCRespiratory Research1465-99212010-03-011113310.1186/1465-9921-11-33Histone deacetylase inhibitor, butyrate, attenuates lipopolysaccharide-induced acute lung injury in miceWang Yun-JieZhao Jin-BoTian FengYan Xiao-LongWang JianNi Yun-FengJiang Tao<p>Abstract</p> <p>Background</p> <p>Histone deacetylase (HDAC) inhibitors, developed as promising anti-tumor drugs, exhibit their anti-inflammatory properties due to their effects on reduction of inflammatory cytokines.</p> <p>Objective</p> <p>To investigate the protective effect of butyrate, a HDAC inhibitor, on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice.</p> <p>Methods</p> <p>ALI was induced in Balb/c mice by intratracheally instillation of LPS (1 mg/kg). Before 1 hour of LPS administration, the mice received butyrate (10 mg/kg) orally. The animals in each group were sacrificed at different time point after LPS administration. Pulmonary histological changes were evaluated by hematoxylin-eosin stain and lung wet/dry weight ratios were observed. Concentrations of interleukin (IL)-1β and tumor necrosis factor (TNF)-α in bronchoalveolar lavage fluid (BALF) and concentrations of nitric oxide (NO) and myeloperoxidase (MPO) activity in lung tissue homogenates were measured by enzyme-linked immunosorbent assay (ELISA). Expression of nuclear factor (NF)-κB p65 in cytoplasm and nucleus was determined by Western blot analysis respectively.</p> <p>Results</p> <p>Pretreatment with butyrate led to significant attenuation of LPS induced evident lung histopathological changes, alveolar hemorrhage, and neutrophils infiltration with evidence of reduced MPO activity. The lung wet/dry weight ratios, as an index of lung edema, were reduced by butyrate administration. Butyrate also repressed the production of TNF-α, IL-1β and NO. Furthermore, the expression of NF-κB p65 in nucleus was markedly suppressed by butyrate pretreatment.</p> <p>Conclusions</p> <p>Butyrate had a protective effect on LPS-induced ALI, which may be related to its effect on suppression of inflammatory cytokines production and NF-κB activation.</p>http://respiratory-research.com/content/11/1/33 |
spellingShingle | Wang Yun-Jie Zhao Jin-Bo Tian Feng Yan Xiao-Long Wang Jian Ni Yun-Feng Jiang Tao Histone deacetylase inhibitor, butyrate, attenuates lipopolysaccharide-induced acute lung injury in mice Respiratory Research |
title | Histone deacetylase inhibitor, butyrate, attenuates lipopolysaccharide-induced acute lung injury in mice |
title_full | Histone deacetylase inhibitor, butyrate, attenuates lipopolysaccharide-induced acute lung injury in mice |
title_fullStr | Histone deacetylase inhibitor, butyrate, attenuates lipopolysaccharide-induced acute lung injury in mice |
title_full_unstemmed | Histone deacetylase inhibitor, butyrate, attenuates lipopolysaccharide-induced acute lung injury in mice |
title_short | Histone deacetylase inhibitor, butyrate, attenuates lipopolysaccharide-induced acute lung injury in mice |
title_sort | histone deacetylase inhibitor butyrate attenuates lipopolysaccharide induced acute lung injury in mice |
url | http://respiratory-research.com/content/11/1/33 |
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