| Exercise training inhibits inflammatory cytokines and more than prevents myocardial dysfunction in rats with sustained beta-adrenergic hyperactivity. | |
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MedLine Citation:
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PMID: 20442263 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Myocardial hypertrophy and dysfunction occur in response to excessive catecholaminergic drive. Adverse cardiac remodelling is associated with activation of proinflammatory cytokines in the myocardium. To test the hypothesis that exercise training can prevent myocardial dysfunction and production of proinflammatory cytokines induced by beta-adrenergic hyperactivity, male Wistar rats were assigned to one of the following four groups: sedentary non-treated (Con); sedentary isoprenaline treated (Iso); exercised non-treated (Ex); and exercised plus isoprenaline (Iso+Ex). Echocardiography, haemodynamic measurements and isolated papillary muscle were used for functional evaluations. Real-time RT-PCR and Western blot were used to quantify tumour necrosis factor alpha, interleukin-6, interleukin-10 and transforming growth factor beta(1) (TGF-beta(1)) in the tissue. NF-B expression in the nucleus was evaluated by immunohistochemical staining. The Iso rats showed a concentric hypertrophy of the left ventricle (LV). These animals exhibited marked increases in LV end-diastolic pressure and impaired myocardial performance in vitro, with a reduction in the developed tension and maximal rate of tension increase and decrease, as well as worsened recruitment of the Frank-Starling mechanism. Both gene and protein levels of tumour necrosis factor alpha and interleukin-6, as well as TGF-beta(1) mRNA, were increased. In addition, the NF-B expression in the Iso group was significantly raised. In the Iso+Ex group, the exercise training had the following effects: (1) it prevented LV hypertrophy; (ii) it improved myocardial contractility; (3) it avoided the increase of proinflammatory cytokines and improved interleukin-10 levels; and (4) it attenuated the increase of TGF-beta(1) mRNA. Thus, exercise training in a model of beta-adrenergic hyperactivity can avoid the adverse remodelling of the LV and inhibit inflammatory cytokines. Moreover, the cardioprotection is related to beneficial effects on myocardial performance. |
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Authors:
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Andrey J Serra; Marília H H Santos; Danilo S Bocalini; Ednei L Antônio; Rozeli F Levy; Alexandra A Santos; Maria L Higuchi; José A Silva; Flávio C Magalhães; Valério G Baraúna; José E Krieger; Paulo J F Tucci |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-05-04 |
Journal Detail:
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Title: The Journal of physiology Volume: 588 ISSN: 1469-7793 ISO Abbreviation: J. Physiol. (Lond.) Publication Date: 2010 Jul |
Date Detail:
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Created Date: 2010-07-02 Completed Date: 2010-10-21 Revised Date: 2011-08-01 |
Medline Journal Info:
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Nlm Unique ID: 0266262 Medline TA: J Physiol Country: England |
Other Details:
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Languages: eng Pagination: 2431-42 Citation Subset: IM |
Affiliation:
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Department of Medicine, Cardiology Division, Federal University of São Paulo, (UNIFESP), São Paulo, SP, Brazil. andreyserra@gmail.com |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adrenergic beta-Agonists
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pharmacology Animals Blotting, Western Cardiomegaly / chemically induced, physiopathology Cardiomyopathies / chemically induced, physiopathology*, prevention & control* Cardiotonic Agents / pharmacology Coronary Circulation / physiology Cytokines / metabolism* Echocardiography Immunohistochemistry Inflammation / metabolism Isoproterenol / pharmacology Male Myocardial Contraction / physiology Myocardium / metabolism NF-kappa B / biosynthesis Physical Conditioning, Animal / physiology* Rats Rats, Wistar Receptors, Adrenergic, beta / drug effects, physiology* Reverse Transcriptase Polymerase Chain Reaction Tumor Necrosis Factor-alpha / metabolism Ventricular Function, Left / physiology |
| Chemical | |
Reg. No./Substance:
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0/Adrenergic beta-Agonists; 0/Cardiotonic Agents; 0/Cytokines; 0/NF-kappa B; 0/Receptors, Adrenergic, beta; 0/Tumor Necrosis Factor-alpha; 7683-59-2/Isoproterenol |
| Comments/Corrections | |
Comment In:
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J Physiol. 2010 Jul 15;588(Pt 14):2525-6
[PMID:
20634182
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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