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Article: Effect of NO donor sodium nitroprusside on lipopolysaccharide induced acute lung injury in rats

TitleEffect of NO donor sodium nitroprusside on lipopolysaccharide induced acute lung injury in rats
Authors
Issue Date2007
PublisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/injury
Citation
Injury, 2007, v. 38 n. 1, p. 53-59 How to Cite?
AbstractNitric oxide (NO) donor-sodium nitroprusside (SNP) mitigates acute lung injury (ALI), but the mechanism of this protection is incompletely known. We investigated the effect of SNP on lipopolysaccharide (LPS)-induced ALI in rats. Forty-eight male Wistar rats were randomly assigned into six groups: the sham-operation group (S group), the LPS instillation group (LPS group), the haemin, a haeme oxygenase-1 (HO-1) inducer, pretreatment group (HM group), the haemin pretreatment plus LPS instillation group (HM + LPS group), the SNP alone and SNP plus LPS treatment groups. Macroscopic and histopathological examinations and immunohistochemistry analysis were performed for the lung specimens 8 h after LPS instillation. Intratracheal administration of LPS induced significant expressions of the inducible isoform of NO synthase (iNOS) and HO-1, while both haemin pretreatment and SNP treatment increased the expression of HO-1 and prevented the expression of iNOS. In the LPS group, the wet-dry weight ratio (W/D), bronchoalveolar lavage fluid (BALF) protein, and lung malondialdehyde (MDA) content were significantly higher than those in the sham-operation group, which were reversed by the pretreatment with haemin or administration of SNP. These results suggest that HO-1 plays a protective role against LPS-induced acute lung injury, which may be achieved at least in part, via inactivating the iNOS/NO system that is involved in the pathophysiological process of LPS-induced acute lung injury. The nitric oxide (NO) donor-SNP ameliorates LPS-induced ALI, which may be related to the induction of HO-1 and the subsequent inhibition of iNOS. © 2006 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/147238
ISSN
2015 Impact Factor: 1.91
2015 SCImago Journal Rankings: 0.982
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXia, Zyen_US
dc.contributor.authorWang, Xyen_US
dc.contributor.authorChen, Xen_US
dc.contributor.authorXia, Zen_US
dc.date.accessioned2012-05-29T06:00:58Z-
dc.date.available2012-05-29T06:00:58Z-
dc.date.issued2007en_US
dc.identifier.citationInjury, 2007, v. 38 n. 1, p. 53-59en_US
dc.identifier.issn0020-1383en_US
dc.identifier.urihttp://hdl.handle.net/10722/147238-
dc.description.abstractNitric oxide (NO) donor-sodium nitroprusside (SNP) mitigates acute lung injury (ALI), but the mechanism of this protection is incompletely known. We investigated the effect of SNP on lipopolysaccharide (LPS)-induced ALI in rats. Forty-eight male Wistar rats were randomly assigned into six groups: the sham-operation group (S group), the LPS instillation group (LPS group), the haemin, a haeme oxygenase-1 (HO-1) inducer, pretreatment group (HM group), the haemin pretreatment plus LPS instillation group (HM + LPS group), the SNP alone and SNP plus LPS treatment groups. Macroscopic and histopathological examinations and immunohistochemistry analysis were performed for the lung specimens 8 h after LPS instillation. Intratracheal administration of LPS induced significant expressions of the inducible isoform of NO synthase (iNOS) and HO-1, while both haemin pretreatment and SNP treatment increased the expression of HO-1 and prevented the expression of iNOS. In the LPS group, the wet-dry weight ratio (W/D), bronchoalveolar lavage fluid (BALF) protein, and lung malondialdehyde (MDA) content were significantly higher than those in the sham-operation group, which were reversed by the pretreatment with haemin or administration of SNP. These results suggest that HO-1 plays a protective role against LPS-induced acute lung injury, which may be achieved at least in part, via inactivating the iNOS/NO system that is involved in the pathophysiological process of LPS-induced acute lung injury. The nitric oxide (NO) donor-SNP ameliorates LPS-induced ALI, which may be related to the induction of HO-1 and the subsequent inhibition of iNOS. © 2006 Elsevier Ltd. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/injuryen_US
dc.relation.ispartofInjuryen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBronchoalveolar Lavage Fluid - Chemistryen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshDrug Evaluation, Preclinicalen_US
dc.subject.meshHeme Oxygenase-1 - Metabolismen_US
dc.subject.meshHemin - Therapeutic Useen_US
dc.subject.meshLipopolysaccharidesen_US
dc.subject.meshLung - Pathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMalondialdehyde - Metabolismen_US
dc.subject.meshNitric Oxide Donors - Therapeutic Useen_US
dc.subject.meshNitric Oxide Synthase Type Ii - Metabolismen_US
dc.subject.meshNitroprusside - Therapeutic Useen_US
dc.subject.meshOrgan Sizeen_US
dc.subject.meshOxygen - Blooden_US
dc.subject.meshPartial Pressureen_US
dc.subject.meshProteins - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshRespiratory Distress Syndrome, Adult - Chemically Induced - Metabolism - Pathology - Prevention & Controlen_US
dc.titleEffect of NO donor sodium nitroprusside on lipopolysaccharide induced acute lung injury in ratsen_US
dc.typeArticleen_US
dc.identifier.emailXia, Z:zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.injury.2006.09.021en_US
dc.identifier.pmid17141778-
dc.identifier.scopuseid_2-s2.0-33845717865en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33845717865&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume38en_US
dc.identifier.issue1en_US
dc.identifier.spage53en_US
dc.identifier.epage59en_US
dc.identifier.isiWOS:000243831100008-
dc.publisher.placeUnited Kingdomen_US

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