Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/922
Type: Artigo de periódico
Title: The Antiapoptotic Effect of Granulocyte Colony-stimulating Factor Reduces Infarct Size and Prevents Heart Failure Development in Rats
Author: BALDO, Marcelo P.
DAVEL, Ana P. C.
DAMAS-SOUZA, Danilo M.
NICOLETTI-CARVALHO, Jose E.
BORDIN, Silvana
CARVALHO, Hernandes F.
RODRIGUES, Sergio L.
ROSSONI, Luciana V.
MILL, Jose G.
Abstract: Background/Aim. Granulocyte colony-stimulating factor (G-CSF) reduces myocardial injury and improves cardiac function after myocardial infarction (MI). We investigated the early alterations provided by G-CSF and the chronic repercussions in infarcted rats. Methods. Male Wistar rats (200-250g) received vehicle (MI) or G-CSF (MI-GCSF) (50 mu g/kg, sc) at 7, 3 and 1 days before MI surgery. Afterwards MI was produced and infarct size was measured 1 and 15 days after surgery. Expression of anti-and proapoptotic proteins was evaluated immediately before surgery. 24 hours after surgery, apoptotic nuclei were evaluated. Two weeks after MI, left ventricular (LV) function was evaluated, followed by in situ LV diastolic pressure-volume evaluation. Results. Infarct size was decreased by 1 day pretreatment before occlusion (36 +/- 2.8 vs. 44 +/- 2.1% in MI; P<0.05) and remained reduced at 15 days after infarction (28 +/- 2.2 vs. 36 +/- 1.4% in MI; P<0.05). G-CSF pretreatment increased Bcl-2 and Bcl-xL protein expression, but did not alter Bax in LV. Apoptotic nuclei were reduced by treatment (Sham: 0.46 +/- 0.42, MI: 15.5 +/- 2.43, MI-GCSF: 5.34 +/- 3.34%; P<0.05). Fifteen days after MI, cardiac function remained preserved in G-CSF pretreated rats. The LV dilation was reduced in MI-G-CSF group as compared to MI rats, being closely associated with infarct size. Conclusion. The early beneficial effects of G-CSF were essentials to preserve cardiac function at a chronic stage of myocardial infarction. Copyright (C) 2011 S. Karger AG, Basel
Subject: G-CSF
Myocardial infarction
Apoptosis
Chamber dilation
Heart failure
Country: Suiça
Editor: KARGER
Citation: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, v.28, n.1, p.33-40, 2011
Rights: fechado
Identifier DOI: 10.1159/000331711
Address: http://dx.doi.org/10.1159/000331711
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Date Issue: 2011
Appears in Collections:IB - Artigos e Materiais de Revistas Científicas

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