File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Hydrogen-rich saline prevents neointima formation after carotid balloon injury by suppressing ROS and the TNF-α/NF-κB pathway

TitleHydrogen-rich saline prevents neointima formation after carotid balloon injury by suppressing ROS and the TNF-α/NF-κB pathway
Authors
Issue Date2012
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis
Citation
Atherosclerosis, 2012, v. 220 n. 2, p. 343-350 How to Cite?
Abstract
Background: Reactive oxygen species (ROS) play a pivotal role in neointima hyperplasia after balloon injury. Molecular hydrogen has emerged as a novel antioxidant and has been proven effective in treating many diseases. Objectives: We aimed to determine the mechanism by which hydrogen affects neointima formation. Methods: We assessed the influence of a hydrogen-rich saline solution (HRSS) by daily injection in rats. Rats were euthanized to evaluate the neointima. ROS, malondialdehyde (MDA) and superoxide dismutase (SOD) and reduced glutathione (GSH), were detected in the injured artery. Macrophage infiltration and the production of inflammatory factors (i.e., IL-6, TNF-α and NF-κB) were also observed. The in vitro effects of hydrogen on vascular smooth muscle cell (VSMC) proliferation were also measured. Results: HRSS decreased the neointima area significantly. The neointima/media ratio was also reduced by HRSS. There was a decline in the number of PCNA-positive cells in the intima treated with HRSS. Meanwhile, HRSS ameliorated the ROS and MDA levels and increased SOD, reduced GSH levels in the injured carotid. In addition, the levels of inflammatory factors, such as IL-6, TNF-α and NF-κB p65, were attenuated by HRSS. In vitro studies also confirmed the anti-proliferative capability of the hydrogen solution and ROS generation in VSMCs induced by PDGF-BB. Conclusion: HRSS may have a protective role in the prevention of neointima hyperplasia and restenosis after angioplasty. HRSS may partially exert its role by neutralizing the local ROS and suppressing the TNF-α/NF-κB pathway. © 2011 Elsevier Ireland Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/168604
ISSN
2013 Impact Factor: 3.971
2013 SCImago Journal Rankings: 1.728
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorQin, ZXen_US
dc.contributor.authorYu, Pen_US
dc.contributor.authorQian, DHen_US
dc.contributor.authorSong, MBen_US
dc.contributor.authorTan, Hen_US
dc.contributor.authorYu, Yen_US
dc.contributor.authorLi, Wen_US
dc.contributor.authorWang, Hen_US
dc.contributor.authorLiu, Jen_US
dc.contributor.authorWang, Qen_US
dc.contributor.authorSun, XJen_US
dc.contributor.authorJiang, Hen_US
dc.contributor.authorZhu, JKen_US
dc.contributor.authorLu, Wen_US
dc.contributor.authorHuang, Len_US
dc.date.accessioned2012-10-08T03:21:27Z-
dc.date.available2012-10-08T03:21:27Z-
dc.date.issued2012en_US
dc.identifier.citationAtherosclerosis, 2012, v. 220 n. 2, p. 343-350en_US
dc.identifier.issn0021-9150en_US
dc.identifier.urihttp://hdl.handle.net/10722/168604-
dc.description.abstractBackground: Reactive oxygen species (ROS) play a pivotal role in neointima hyperplasia after balloon injury. Molecular hydrogen has emerged as a novel antioxidant and has been proven effective in treating many diseases. Objectives: We aimed to determine the mechanism by which hydrogen affects neointima formation. Methods: We assessed the influence of a hydrogen-rich saline solution (HRSS) by daily injection in rats. Rats were euthanized to evaluate the neointima. ROS, malondialdehyde (MDA) and superoxide dismutase (SOD) and reduced glutathione (GSH), were detected in the injured artery. Macrophage infiltration and the production of inflammatory factors (i.e., IL-6, TNF-α and NF-κB) were also observed. The in vitro effects of hydrogen on vascular smooth muscle cell (VSMC) proliferation were also measured. Results: HRSS decreased the neointima area significantly. The neointima/media ratio was also reduced by HRSS. There was a decline in the number of PCNA-positive cells in the intima treated with HRSS. Meanwhile, HRSS ameliorated the ROS and MDA levels and increased SOD, reduced GSH levels in the injured carotid. In addition, the levels of inflammatory factors, such as IL-6, TNF-α and NF-κB p65, were attenuated by HRSS. In vitro studies also confirmed the anti-proliferative capability of the hydrogen solution and ROS generation in VSMCs induced by PDGF-BB. Conclusion: HRSS may have a protective role in the prevention of neointima hyperplasia and restenosis after angioplasty. HRSS may partially exert its role by neutralizing the local ROS and suppressing the TNF-α/NF-κB pathway. © 2011 Elsevier Ireland Ltd.en_US
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosisen_US
dc.relation.ispartofAtherosclerosisen_US
dc.subject.meshAngioplasty, Balloonen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntioxidants - Administration & Dosage - Pharmacologyen_US
dc.subject.meshCarotid Arteries - Drug Effects - Immunology - Metabolism - Pathologyen_US
dc.subject.meshCarotid Artery Injuries - Drug Therapy - Etiology - Immunology - Metabolism - Pathologyen_US
dc.subject.meshCell Proliferation - Drug Effectsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshGlutathione - Metabolismen_US
dc.subject.meshHydrogen - Administration & Dosage - Blood - Pharmacologyen_US
dc.subject.meshInflammation Mediators - Metabolismen_US
dc.subject.meshInjections, Intraperitonealen_US
dc.subject.meshInterleukin-6 - Metabolismen_US
dc.subject.meshMalondialdehyde - Metabolismen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Immunology - Injuries - Metabolismen_US
dc.subject.meshMyocytes, Smooth Muscle - Drug Effects - Immunology - Metabolismen_US
dc.subject.meshNf-Kappa B - Metabolismen_US
dc.subject.meshProto-Oncogene Proteins C-Sis - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReactive Oxygen Species - Metabolismen_US
dc.subject.meshSignal Transduction - Drug Effectsen_US
dc.subject.meshSodium Chloride - Administration & Dosage - Blood - Pharmacologyen_US
dc.subject.meshSuperoxide Dismutase - Metabolismen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Metabolismen_US
dc.subject.meshTunica Intima - Drug Effects - Immunology - Metabolism - Pathologyen_US
dc.titleHydrogen-rich saline prevents neointima formation after carotid balloon injury by suppressing ROS and the TNF-α/NF-κB pathwayen_US
dc.typeArticleen_US
dc.identifier.emailLu, W:luwei@hku.hken_US
dc.identifier.authorityLu, W=rp00754en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.atherosclerosis.2011.11.002en_US
dc.identifier.pmid22153150en_US
dc.identifier.scopuseid_2-s2.0-84855937906en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84855937906&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume220en_US
dc.identifier.issue2en_US
dc.identifier.spage343en_US
dc.identifier.epage350en_US
dc.identifier.isiWOS:000299319100010-
dc.publisher.placeIrelanden_US
dc.identifier.scopusauthoridQin, ZX=35211223400en_US
dc.identifier.scopusauthoridYu, P=43561946600en_US
dc.identifier.scopusauthoridQian, DH=25926032100en_US
dc.identifier.scopusauthoridSong, MB=12763887800en_US
dc.identifier.scopusauthoridTan, H=35485920800en_US
dc.identifier.scopusauthoridYu, Y=34979429100en_US
dc.identifier.scopusauthoridLi, W=54412615200en_US
dc.identifier.scopusauthoridWang, H=54413162200en_US
dc.identifier.scopusauthoridLiu, J=54412617200en_US
dc.identifier.scopusauthoridWang, Q=54413224300en_US
dc.identifier.scopusauthoridSun, XJ=54896871300en_US
dc.identifier.scopusauthoridJiang, H=34769714800en_US
dc.identifier.scopusauthoridZhu, JK=54898596000en_US
dc.identifier.scopusauthoridLu, W=27868087600en_US
dc.identifier.scopusauthoridHuang, L=34769889600en_US
dc.identifier.citeulike10029679-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats