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Article: Ischaemic post-conditioning protects lung from ischaemia-reperfusion injury by up-regulation of haeme oxygenase-1

TitleIschaemic post-conditioning protects lung from ischaemia-reperfusion injury by up-regulation of haeme oxygenase-1
Authors
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
Citation
Injury, 2010, v. 41 n. 5, p. 510-516 How to Cite?
Abstract
Objective: 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.
Persistent Identifierhttp://hdl.handle.net/10722/58171
ISSN
2013 Impact Factor: 2.462
ISI Accession Number ID
References

 

Author Affiliations
  1. Hubei General Hospital
  2. The University of Hong Kong
  3. Sun Yat-Sen University
DC FieldValueLanguage
dc.contributor.authorXia, Zyen_HK
dc.contributor.authorGao, Jen_HK
dc.contributor.authorAncharaz, AKen_HK
dc.contributor.authorLiu, Kxen_HK
dc.contributor.authorXia, Zen_HK
dc.contributor.authorLuo, Ten_HK
dc.date.accessioned2010-05-31T03:25:05Z-
dc.date.available2010-05-31T03:25:05Z-
dc.date.issued2010en_HK
dc.identifier.citationInjury, 2010, v. 41 n. 5, p. 510-516en_HK
dc.identifier.issn0020-1383en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58171-
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.en_HK
dc.languageengen_HK
dc.publisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/injuryen_HK
dc.relation.ispartofInjuryen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectHaeme oxygenase-1en_HK
dc.subjectIschaemia-reperfusion injuryen_HK
dc.subjectLungen_HK
dc.subjectPost-conditioningen_HK
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.titleIschaemic post-conditioning protects lung from ischaemia-reperfusion injury by up-regulation of haeme oxygenase-1en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0020-1383&volume=41&issue=5&spage=510&epage=516&date=2010&atitle=Ischaemic+post-conditioning+protects+lung+from+ischaemia-reperfusion+injury+by+up-regulation+of+haeme+oxygenase-1en_HK
dc.identifier.emailXia, Z:zyxia@hkucc.hku.hken_HK
dc.identifier.authorityXia, Z=rp00532en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1016/j.injury.2009.03.002en_HK
dc.identifier.pmid19524915en_HK
dc.identifier.scopuseid_2-s2.0-77950022168en_HK
dc.identifier.hkuros162381en_HK
dc.identifier.hkuros171292-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77950022168&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume41en_HK
dc.identifier.issue5en_HK
dc.identifier.spage510en_HK
dc.identifier.epage516en_HK
dc.identifier.isiWOS:000277699800016-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.citeulike5072297-

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