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
2011 Impact Factor: 3.794
2011 SCImago Journal Rankings: 0.372
DOIhttp://dx.doi.org/10.1016/j.atherosclerosis.2011.11.002
ReferencesReferences in Scopus
DC Field
Value
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
2011 Impact Factor: 3.794
2011 SCImago Journal Rankings: 0.372
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
Author Affiliations
  1. Third Military Medical University
  2. Second Military Medical University