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Article: Hydrogen-rich saline prevents neointima formation after carotid balloon injury by suppressing ROS and the TNF-α/NF-κB pathway
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TitleHydrogen-rich saline prevents neointima formation after carotid balloon injury by suppressing ROS and the TNF-α/NF-κB pathway
 
AuthorsQin, ZX1
Yu, P1
Qian, DH1
Song, MB1
Tan, H1
Yu, Y1
Li, W1
Wang, H1
Liu, J1
Wang, Q1
Sun, XJ2
Jiang, H1
Zhu, JK1
Lu, W1
Huang, L1
 
Issue Date2012
 
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis
 
CitationAtherosclerosis, 2012, v. 220 n. 2, p. 343-350 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.atherosclerosis.2011.11.002
 
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.
 
ISSN0021-9150
2012 Impact Factor: 3.706
2012 SCImago Journal Rankings: 1.388
 
DOIhttp://dx.doi.org/10.1016/j.atherosclerosis.2011.11.002
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorQin, ZX
 
dc.contributor.authorYu, P
 
dc.contributor.authorQian, DH
 
dc.contributor.authorSong, MB
 
dc.contributor.authorTan, H
 
dc.contributor.authorYu, Y
 
dc.contributor.authorLi, W
 
dc.contributor.authorWang, H
 
dc.contributor.authorLiu, J
 
dc.contributor.authorWang, Q
 
dc.contributor.authorSun, XJ
 
dc.contributor.authorJiang, H
 
dc.contributor.authorZhu, JK
 
dc.contributor.authorLu, W
 
dc.contributor.authorHuang, L
 
dc.date.accessioned2012-10-08T03:21:27Z
 
dc.date.available2012-10-08T03:21:27Z
 
dc.date.issued2012
 
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.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationAtherosclerosis, 2012, v. 220 n. 2, p. 343-350 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.atherosclerosis.2011.11.002
 
dc.identifier.citeulike10029679
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.atherosclerosis.2011.11.002
 
dc.identifier.epage350
 
dc.identifier.issn0021-9150
2012 Impact Factor: 3.706
2012 SCImago Journal Rankings: 1.388
 
dc.identifier.issue2
 
dc.identifier.pmid22153150
 
dc.identifier.scopuseid_2-s2.0-84855937906
 
dc.identifier.spage343
 
dc.identifier.urihttp://hdl.handle.net/10722/168604
 
dc.identifier.volume220
 
dc.languageeng
 
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis
 
dc.publisher.placeIreland
 
dc.relation.ispartofAtherosclerosis
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAngioplasty, Balloon
 
dc.subject.meshAnimals
 
dc.subject.meshAntioxidants - Administration & Dosage - Pharmacology
 
dc.subject.meshCarotid Arteries - Drug Effects - Immunology - Metabolism - Pathology
 
dc.subject.meshCarotid Artery Injuries - Drug Therapy - Etiology - Immunology - Metabolism - Pathology
 
dc.subject.meshCell Proliferation - Drug Effects
 
dc.subject.meshCells, Cultured
 
dc.subject.meshDisease Models, Animal
 
dc.subject.meshGlutathione - Metabolism
 
dc.subject.meshHydrogen - Administration & Dosage - Blood - Pharmacology
 
dc.subject.meshInflammation Mediators - Metabolism
 
dc.subject.meshInjections, Intraperitoneal
 
dc.subject.meshInterleukin-6 - Metabolism
 
dc.subject.meshMalondialdehyde - Metabolism
 
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Immunology - Injuries - Metabolism
 
dc.subject.meshMyocytes, Smooth Muscle - Drug Effects - Immunology - Metabolism
 
dc.subject.meshNf-Kappa B - Metabolism
 
dc.subject.meshProto-Oncogene Proteins C-Sis - Metabolism
 
dc.subject.meshRats
 
dc.subject.meshRats, Sprague-Dawley
 
dc.subject.meshReactive Oxygen Species - Metabolism
 
dc.subject.meshSignal Transduction - Drug Effects
 
dc.subject.meshSodium Chloride - Administration & Dosage - Blood - Pharmacology
 
dc.subject.meshSuperoxide Dismutase - Metabolism
 
dc.subject.meshTime Factors
 
dc.subject.meshTumor Necrosis Factor-Alpha - Metabolism
 
dc.subject.meshTunica Intima - Drug Effects - Immunology - Metabolism - Pathology
 
dc.titleHydrogen-rich saline prevents neointima formation after carotid balloon injury by suppressing ROS and the TNF-α/NF-κB pathway
 
dc.typeArticle
 
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<contributor.author>Tan, H</contributor.author>
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<description.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-&#945; and NF-&#954;B) 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-&#945; and NF-&#954;B 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-&#945;/NF-&#954;B pathway. &#169; 2011 Elsevier Ireland Ltd.</description.abstract>
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<subject.mesh>Superoxide Dismutase - Metabolism</subject.mesh>
<subject.mesh>Time Factors</subject.mesh>
<subject.mesh>Tumor Necrosis Factor-Alpha - Metabolism</subject.mesh>
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Author Affiliations
  1. Third Military Medical University
  2. Second Military Medical University