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Effect of salidroside on lung injury by upregulating peroxisome proliferator-activated receptor γ expression in septic rats
Successful drug treatment for sepsis-related acute lung injury (ALI) remains a major clinical problem. Thus, the aim of the present study was to investigate the beneficial effects of salidroside on ameliorating cecal ligation and puncture (CLP)-induced lung inflammation. Rats underwent CLP surgery t...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4043580/ https://www.ncbi.nlm.nih.gov/pubmed/24926325 http://dx.doi.org/10.3892/etm.2014.1629 |
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author | LIU, MING-WEI SU, MEI-XIAN QIN, LAN-FANG LIU, XU TIAN, MAO-LI ZHANG, WEI WANG, YUN-HUI |
author_facet | LIU, MING-WEI SU, MEI-XIAN QIN, LAN-FANG LIU, XU TIAN, MAO-LI ZHANG, WEI WANG, YUN-HUI |
author_sort | LIU, MING-WEI |
collection | PubMed |
description | Successful drug treatment for sepsis-related acute lung injury (ALI) remains a major clinical problem. Thus, the aim of the present study was to investigate the beneficial effects of salidroside on ameliorating cecal ligation and puncture (CLP)-induced lung inflammation. Rats underwent CLP surgery to induce ALI and 800 mg/kg salidroside (i.v.) was administered 24 h after the CLP challenge. Subsequently, biochemical changes in the blood and lung tissues, as well as morphological and histological alterations in the lungs, that were associated with inflammation and injury were analysed. CLP was shown to significantly increase the serum levels of plasma tumour necrosis factor-α and interleukin-6, -1β and-10. In addition, CLP increased pulmonary oedema, thickened the alveolar septa and caused inflammation in the lung cells. These changes were ameliorated by the administration of 800 mg/kg salidroside (i.v.) 24 h after the CLP challenge. This post-treatment drug administration also significantly attenuated the lipopolysaccharide-induced activation of nuclear factor-κβ and increased the release of peroxisome proliferator-activated receptor γ in the lung tissue. Therefore, salidroside administered following the induction of ALI by CLP significantly prevented and reversed lung tissue injuries. The positive post-treatment effects of salidroside administration indicated that salidroside may be a potential candidate for the management of lung inflammation in CLP-induced endotoxemia and septic shock. |
format | Online Article Text |
id | pubmed-4043580 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-40435802014-06-12 Effect of salidroside on lung injury by upregulating peroxisome proliferator-activated receptor γ expression in septic rats LIU, MING-WEI SU, MEI-XIAN QIN, LAN-FANG LIU, XU TIAN, MAO-LI ZHANG, WEI WANG, YUN-HUI Exp Ther Med Articles Successful drug treatment for sepsis-related acute lung injury (ALI) remains a major clinical problem. Thus, the aim of the present study was to investigate the beneficial effects of salidroside on ameliorating cecal ligation and puncture (CLP)-induced lung inflammation. Rats underwent CLP surgery to induce ALI and 800 mg/kg salidroside (i.v.) was administered 24 h after the CLP challenge. Subsequently, biochemical changes in the blood and lung tissues, as well as morphological and histological alterations in the lungs, that were associated with inflammation and injury were analysed. CLP was shown to significantly increase the serum levels of plasma tumour necrosis factor-α and interleukin-6, -1β and-10. In addition, CLP increased pulmonary oedema, thickened the alveolar septa and caused inflammation in the lung cells. These changes were ameliorated by the administration of 800 mg/kg salidroside (i.v.) 24 h after the CLP challenge. This post-treatment drug administration also significantly attenuated the lipopolysaccharide-induced activation of nuclear factor-κβ and increased the release of peroxisome proliferator-activated receptor γ in the lung tissue. Therefore, salidroside administered following the induction of ALI by CLP significantly prevented and reversed lung tissue injuries. The positive post-treatment effects of salidroside administration indicated that salidroside may be a potential candidate for the management of lung inflammation in CLP-induced endotoxemia and septic shock. D.A. Spandidos 2014-06 2014-03-21 /pmc/articles/PMC4043580/ /pubmed/24926325 http://dx.doi.org/10.3892/etm.2014.1629 Text en Copyright © 2014, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. |
spellingShingle | Articles LIU, MING-WEI SU, MEI-XIAN QIN, LAN-FANG LIU, XU TIAN, MAO-LI ZHANG, WEI WANG, YUN-HUI Effect of salidroside on lung injury by upregulating peroxisome proliferator-activated receptor γ expression in septic rats |
title | Effect of salidroside on lung injury by upregulating peroxisome proliferator-activated receptor γ expression in septic rats |
title_full | Effect of salidroside on lung injury by upregulating peroxisome proliferator-activated receptor γ expression in septic rats |
title_fullStr | Effect of salidroside on lung injury by upregulating peroxisome proliferator-activated receptor γ expression in septic rats |
title_full_unstemmed | Effect of salidroside on lung injury by upregulating peroxisome proliferator-activated receptor γ expression in septic rats |
title_short | Effect of salidroside on lung injury by upregulating peroxisome proliferator-activated receptor γ expression in septic rats |
title_sort | effect of salidroside on lung injury by upregulating peroxisome proliferator-activated receptor γ expression in septic rats |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4043580/ https://www.ncbi.nlm.nih.gov/pubmed/24926325 http://dx.doi.org/10.3892/etm.2014.1629 |
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