| Apocynin attenuates pressure overload-induced cardiac hypertrophy in rats by reducing levels of reactive oxygen species. | |
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MedLine Citation:
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PMID: 20651822 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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It has been shown that angiotensin II (Ang II) is involved in cardiac remodeling mediated by NADPH oxidase-dependent reactive oxygen species (ROS). Accordingly, NADPH oxidase-dependent ROS may play a role in cardiac hypertrophy induced by pressure overload. In the present study, we sought to determine whether inhibition of NADPH oxidase prevents cardiac hypertrophy. After abdominal aorta banding to induce cardiac hypertrophy, rats were treated for 8 weeks with apocynin (Apo) or captopril (Cap). Measures of cardiac hypertrophy were evaluated. Treatment with Cap or Apo reduced the left ventricle/body weight ratio (LV/BW), LV transnuclear myocyte diameter, and atrial natriuretic factor (ANF) mRNA expression relative to those of untreated rats subjected to aorta banding. The activity of NADPH oxidase and the ROS levels were decreased in treated animals. Cap, but not Apo, decreased Ang II levels and inhibited expression of p22phox and p67phox in LVs. In conclusion, local expression of Ang II appears to contribute to pressure overload-induced cardiac hypertrophy by upregulating NADPH oxidase expression and promoting ROS synthesis. Inhibition of NADPH oxidase and elimination of ROS may prevent or repair damage due to cardiac hypertrophy. |
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Authors:
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Jinjun Liu; Juan Zhou; Wenjiao An; Yuanxi Lin; Yubai Yang; Weijin Zang |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Canadian journal of physiology and pharmacology Volume: 88 ISSN: 1205-7541 ISO Abbreviation: Can. J. Physiol. Pharmacol. Publication Date: 2010 Jul |
Date Detail:
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Created Date: 2010-07-23 Completed Date: 2010-11-05 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0372712 Medline TA: Can J Physiol Pharmacol Country: Canada |
Other Details:
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Languages: eng Pagination: 745-52 Citation Subset: IM |
Affiliation:
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Department of Physiology and Pathophysiology, School of Medicine, Xi'an Jiaotong University, Xi'an 710061, Shaanxi, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acetophenones
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pharmacology* Angiotensin II / blood, metabolism Animals Antioxidants / pharmacology Atrial Natriuretic Factor / genetics, metabolism Base Sequence Captopril / pharmacology Cardiomegaly / drug therapy*, genetics, pathology, physiopathology* DNA Primers / genetics Enzyme Inhibitors / pharmacology Male NADPH Oxidase / antagonists & inhibitors, genetics, metabolism Phosphoproteins / genetics, metabolism RNA, Messenger / genetics, metabolism Rats Rats, Sprague-Dawley Reactive Oxygen Species / metabolism* |
| Chemical | |
Reg. No./Substance:
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0/Acetophenones; 0/Antioxidants; 0/DNA Primers; 0/Enzyme Inhibitors; 0/Phosphoproteins; 0/RNA, Messenger; 0/Reactive Oxygen Species; 0/atrial natriuretic peptide, rat; 0/neutrophil cytosol factor 67K; 11128-99-7/Angiotensin II; 498-02-2/acetovanillone; 62571-86-2/Captopril; 85637-73-6/Atrial Natriuretic Factor; EC 1.6.3.1/NADPH Oxidase; EC 1.6.3.1/p22-phox protein, rat |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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