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Article: Ischemic postconditioning attenuates lung reperfusion injury and reduces systemic proinflammatory cytokine release via heme oxygenase 1

TitleIschemic postconditioning attenuates lung reperfusion injury and reduces systemic proinflammatory cytokine release via heme oxygenase 1
Authors
Keywordsheme oxygenase 1
ischemic postconditioning
lung ischemia reperfusion
proinflammatory cytokines
Issue Date2011
PublisherElsevier Inc.. The Journal's web site is located at http://www.elsevier.com/locate/jsre
Citation
Journal Of Surgical Research, 2011, v. 166 n. 2, p. e157-e164 How to Cite?
AbstractObjective: Systemic inflammatory response following ischemia-reperfusion injury (IRI) to a specific organ may cause injuries in multiple remote organs. The emergence of ischemic postconditioning (IPO) provides a potential method for experimentally and clinically attenuating various types of organ postischemic injuries. We have shown that IPO can attenuate lung IRI by up-regulating the protein expression of heme oxygenase-1(HO-1). This study tested the hypothesis that IPO attenuates systemic inflammatory responses following lung IRI by activating HO-1. Methods: Anaesthetized 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 ischemia-reperfusion (IR) group (40 min of left-lung ischemia and 120 min of reperfusion), the IPO group (three successive cycles of 30-s reperfusion per 30-s occlusion before restoring full perfusion), and the zinc protoporphyrin IX (ZnP) plus IPO group (ZnP, an inhibitor of HO-1, was injected intraperitoneally at 20 mg/kg 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 histologic and biochemical changes. The lung tissue and plasma levels of lipid peroxidation were determined by measuring the contents of malondialdehyde (MDA) production. Protein expression of HO-1 was determined by Western blotting. Pulmonary neutrophil was counted. Lung tissue myeloperoxidase (MPO) activity as well as plasma levels of proinflammatory cytokines tumor necrosis factor-α (TNF-α), interleukines 6 and 8 (IL-6, IL-8) were determined by spectrophotography. Results: Lung ischemia-reperfusion led to severe lung pathologic morphologic changes and increased pulmonary MDA production, neutrophil count, and MPO activity and reduced arterial oxygen partial pressure (all P < 0.05 IR versus sham), accompanied with a compensatory increase in HO-1 protein and activity. Plasma levels of TNF-α, IL-6, and IL-8 were increased in the IR group (all P < 0.05 versus sham). IPO attenuated or prevented all the above changes, except that it further increased lung HO-1 activity. Treatment with ZnP abolished all the protective effects of postconditioning. Conclusion: Postconditioning attenuated pulmonary neutrophil accumulation and activation and lung IRI and reduced systemic inflammatory responses by activating HO-1. © 2011 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/138929
ISSN
2015 Impact Factor: 2.198
2015 SCImago Journal Rankings: 0.928
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Science Foundation of China (NSFC)30872447
30672033
Funding Information:

This study is supported in part by the National Natural Science Foundation of China (NSFC) (no. 30872447, 30672033).

References

 

DC FieldValueLanguage
dc.contributor.authorXu, Ben_HK
dc.contributor.authorGao, Xen_HK
dc.contributor.authorXu, Jen_HK
dc.contributor.authorLei, Sen_HK
dc.contributor.authorXia, ZYen_HK
dc.contributor.authorXu, Yen_HK
dc.contributor.authorXia, Zen_HK
dc.date.accessioned2011-09-23T05:42:16Z-
dc.date.available2011-09-23T05:42:16Z-
dc.date.issued2011en_HK
dc.identifier.citationJournal Of Surgical Research, 2011, v. 166 n. 2, p. e157-e164en_HK
dc.identifier.issn0022-4804en_HK
dc.identifier.urihttp://hdl.handle.net/10722/138929-
dc.description.abstractObjective: Systemic inflammatory response following ischemia-reperfusion injury (IRI) to a specific organ may cause injuries in multiple remote organs. The emergence of ischemic postconditioning (IPO) provides a potential method for experimentally and clinically attenuating various types of organ postischemic injuries. We have shown that IPO can attenuate lung IRI by up-regulating the protein expression of heme oxygenase-1(HO-1). This study tested the hypothesis that IPO attenuates systemic inflammatory responses following lung IRI by activating HO-1. Methods: Anaesthetized 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 ischemia-reperfusion (IR) group (40 min of left-lung ischemia and 120 min of reperfusion), the IPO group (three successive cycles of 30-s reperfusion per 30-s occlusion before restoring full perfusion), and the zinc protoporphyrin IX (ZnP) plus IPO group (ZnP, an inhibitor of HO-1, was injected intraperitoneally at 20 mg/kg 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 histologic and biochemical changes. The lung tissue and plasma levels of lipid peroxidation were determined by measuring the contents of malondialdehyde (MDA) production. Protein expression of HO-1 was determined by Western blotting. Pulmonary neutrophil was counted. Lung tissue myeloperoxidase (MPO) activity as well as plasma levels of proinflammatory cytokines tumor necrosis factor-α (TNF-α), interleukines 6 and 8 (IL-6, IL-8) were determined by spectrophotography. Results: Lung ischemia-reperfusion led to severe lung pathologic morphologic changes and increased pulmonary MDA production, neutrophil count, and MPO activity and reduced arterial oxygen partial pressure (all P < 0.05 IR versus sham), accompanied with a compensatory increase in HO-1 protein and activity. Plasma levels of TNF-α, IL-6, and IL-8 were increased in the IR group (all P < 0.05 versus sham). IPO attenuated or prevented all the above changes, except that it further increased lung HO-1 activity. Treatment with ZnP abolished all the protective effects of postconditioning. Conclusion: Postconditioning attenuated pulmonary neutrophil accumulation and activation and lung IRI and reduced systemic inflammatory responses by activating HO-1. © 2011 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_US
dc.publisherElsevier Inc.. The Journal's web site is located at http://www.elsevier.com/locate/jsreen_HK
dc.relation.ispartofJournal of Surgical Researchen_HK
dc.subjectheme oxygenase 1en_HK
dc.subjectischemic postconditioningen_HK
dc.subjectlung ischemia reperfusionen_HK
dc.subjectproinflammatory cytokinesen_HK
dc.subject.meshBlood Gas Analysis-
dc.subject.meshCytokines - blood-
dc.subject.meshHeme Oxygenase (Decyclizing) - immunology - metabolism-
dc.subject.meshIschemic Preconditioning - methods-
dc.subject.meshReperfusion Injury - immunology - pathology - prevention and control-
dc.titleIschemic postconditioning attenuates lung reperfusion injury and reduces systemic proinflammatory cytokine release via heme oxygenase 1en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-4804&volume=166&issue=2&spage=e157&epage=e164&date=2011&atitle=Ischemic+postconditioning+attenuates+lung+reperfusion+injury+and+reduces+systemic+proinflammatory+cytokine+release+via+heme+oxygenase+1-
dc.identifier.emailXia, Z:zyxia@hkucc.hku.hken_HK
dc.identifier.authorityXia, Z=rp00532en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.jss.2010.11.902en_HK
dc.identifier.pmid21227458-
dc.identifier.scopuseid_2-s2.0-79952489004en_HK
dc.identifier.hkuros193432en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79952489004&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume166en_HK
dc.identifier.issue2en_HK
dc.identifier.spagee157en_HK
dc.identifier.epagee164en_HK
dc.identifier.isiWOS:000288168300010-
dc.publisher.placeUnited Statesen_HK

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