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Article: Ischaemic post-conditioning protects lung from ischaemia-reperfusion injury by up-regulation of haeme oxygenase-1
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TitleIschaemic post-conditioning protects lung from ischaemia-reperfusion injury by up-regulation of haeme oxygenase-1
 
AuthorsXia, Zy1
Gao, J1
Ancharaz, AK1
Liu, Kx3
Xia, Z2
Luo, T1
 
KeywordsHaeme oxygenase-1
Ischaemia-reperfusion injury
Lung
Post-conditioning
 
Issue Date2010
 
PublisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/injury
 
CitationInjury, 2010, v. 41 n. 5, p. 510-516 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.injury.2009.03.002
 
AbstractObjective: The emergence of ischaemic post-conditioning (IPO) provides a potential method for experimentally and clinically attenuating various types of organ injuries. There has been little work, however, examining its effects in the setting of lung ischaemia reperfusion (IR). The stress protein, haeme oxygenase-1 (HO-1), has been found to exert a potent, protective role in a variety of lung injury models. In this study, we hypothesised that the induction of HO-1 by IPO plays a protective role against the deleterious effects of IR in the lung. Methods: Anaesthetised and mechanically ventilated adult Sprague-Dawley rats were randomly assigned to one of the following groups (n = 8 each): the sham-operated control group, the IR group (40 min of left-lung ischaemia and 105 min of reperfusion), the IPO group (three successive cycles of 30-s reperfusion per 30-s occlusion before restoring full perfusion) and the ZnPPIX + IPO group (ZnPPIX, an inhibitor of HO-1, was injected intra-peritoneally at 20 mg kg -1 24 h prior to the experiment and the rest of the procedures were similar to that of the IPO group). Lung injury was assessed by arterial blood gas analysis, wet-to-dry lung weight ratio and tissue histological changes. The extent of lipid peroxidation was determined by measuring plasma levels of malondialdehyde (MDA) production. Expression of HO-1 was determined by immunohistochemistry. Results: Lung IR resulted in a significant reduction of PaO 2 (data in IR, P < 0.05 vs. data in sham) and increase of lung wet-to-dry weight ratio, accompanied with increased MDA production and severe lung pathological morphological changes as well as a compensatory increase in HO-1 protein expression, as compared with sham (All P < 0.05). IPO markedly attenuated all the above pathological changes seen in the IR group and further increased HO-1 expression. Treatment with ZnPPIX abolished all the protective effects of post-conditioning. Conclusion: It may be concluded that IPO protects IR-induced lung injury via induction of HO-1. © 2009 Elsevier Ltd. All rights reserved.
 
ISSN0020-1383
2012 Impact Factor: 1.931
2012 SCImago Journal Rankings: 0.834
 
DOIhttp://dx.doi.org/10.1016/j.injury.2009.03.002
 
ISI Accession Number IDWOS:000277699800016
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorXia, Zy
 
dc.contributor.authorGao, J
 
dc.contributor.authorAncharaz, AK
 
dc.contributor.authorLiu, Kx
 
dc.contributor.authorXia, Z
 
dc.contributor.authorLuo, T
 
dc.date.accessioned2010-05-31T03:25:05Z
 
dc.date.available2010-05-31T03:25:05Z
 
dc.date.issued2010
 
dc.description.abstractObjective: The emergence of ischaemic post-conditioning (IPO) provides a potential method for experimentally and clinically attenuating various types of organ injuries. There has been little work, however, examining its effects in the setting of lung ischaemia reperfusion (IR). The stress protein, haeme oxygenase-1 (HO-1), has been found to exert a potent, protective role in a variety of lung injury models. In this study, we hypothesised that the induction of HO-1 by IPO plays a protective role against the deleterious effects of IR in the lung. Methods: Anaesthetised and mechanically ventilated adult Sprague-Dawley rats were randomly assigned to one of the following groups (n = 8 each): the sham-operated control group, the IR group (40 min of left-lung ischaemia and 105 min of reperfusion), the IPO group (three successive cycles of 30-s reperfusion per 30-s occlusion before restoring full perfusion) and the ZnPPIX + IPO group (ZnPPIX, an inhibitor of HO-1, was injected intra-peritoneally at 20 mg kg -1 24 h prior to the experiment and the rest of the procedures were similar to that of the IPO group). Lung injury was assessed by arterial blood gas analysis, wet-to-dry lung weight ratio and tissue histological changes. The extent of lipid peroxidation was determined by measuring plasma levels of malondialdehyde (MDA) production. Expression of HO-1 was determined by immunohistochemistry. Results: Lung IR resulted in a significant reduction of PaO 2 (data in IR, P < 0.05 vs. data in sham) and increase of lung wet-to-dry weight ratio, accompanied with increased MDA production and severe lung pathological morphological changes as well as a compensatory increase in HO-1 protein expression, as compared with sham (All P < 0.05). IPO markedly attenuated all the above pathological changes seen in the IR group and further increased HO-1 expression. Treatment with ZnPPIX abolished all the protective effects of post-conditioning. Conclusion: It may be concluded that IPO protects IR-induced lung injury via induction of HO-1. © 2009 Elsevier Ltd. All rights reserved.
 
dc.description.naturepostprint
 
dc.identifier.citationInjury, 2010, v. 41 n. 5, p. 510-516 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.injury.2009.03.002
 
dc.identifier.citeulike5072297
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.injury.2009.03.002
 
dc.identifier.epage516
 
dc.identifier.hkuros162381
 
dc.identifier.isiWOS:000277699800016
 
dc.identifier.issn0020-1383
2012 Impact Factor: 1.931
2012 SCImago Journal Rankings: 0.834
 
dc.identifier.issue5
 
dc.identifier.openurl
 
dc.identifier.pmid19524915
 
dc.identifier.scopuseid_2-s2.0-77950022168
 
dc.identifier.spage510
 
dc.identifier.urihttp://hdl.handle.net/10722/58171
 
dc.identifier.volume41
 
dc.languageeng
 
dc.publisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/injury
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofInjury
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subject.meshEnzyme Inhibitors - pharmacology
 
dc.subject.meshHeme Oxygenase-1 - antagonists and inhibitors - physiology
 
dc.subject.meshLung - blood supply
 
dc.subject.meshReperfusion - methods
 
dc.subject.meshReperfusion Injury - prevention and control
 
dc.subjectHaeme oxygenase-1
 
dc.subjectIschaemia-reperfusion injury
 
dc.subjectLung
 
dc.subjectPost-conditioning
 
dc.titleIschaemic post-conditioning protects lung from ischaemia-reperfusion injury by up-regulation of haeme oxygenase-1
 
dc.typeArticle
 
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Author Affiliations
  1. Hubei General Hospital
  2. The University of Hong Kong
  3. Sun Yat-Sen University