Document Detail

Bone marrow derived cells decrease inflammation but not oxidative stress in an experimental model of acute myocardial infarction.
MedLine Citation:
PMID:  20970437     Owner:  NLM     Status:  MEDLINE    
AIMS: Bone marrow cell (BMC) therapy is thought to exert beneficial effects on the infarcted heart. We assessed cardiac function and its correlation with redox status and inflammation in cardiac tissue early post-AMI in rats treated with BMC.
MAIN METHODS: Male Wistar rats (8-week-old) were randomized into four groups: Sham-operated (S); AMI; S+treatment (ST) and AMI+treatment (AMIT). Therapy with BMC was carried out immediately post-experimental left anterior coronary artery ligation induced-AMI, and assessments made 48h later. Cardiac function and morphometrics were evaluated by echocardiographyc parameters in vivo. Cardiac tissue tumor necrosis factor (TNF)-α and interleukin (IL)-6 were measured by Western Blot. Oxidative stress parameters including reduced (GSH) and oxidized (GSSG) glutathione ratio, hydrogen peroxide level, lipid and protein oxidation, superoxide dismutase, catalase and glutathione peroxidase activities were measured spectrophotometrically.
KEY FINDINGS: Ejection fraction was lower in infarcted groups and did not improve in BMC-treated animals: AMI (51±5%) vs. S (74±7%) and AMIT (56±10%) vs. ST groups (73±3%). Both TNF-α and IL-6 myocardial expression increased post-AMI and were reduced following BMC therapy. Nonetheless, there was a decrease in GSH/GSSG ratio in infarcted groups which was greater in BMC-treated groups: AMI (8.21±3.8) vs. S (14.61±3.4) and AMIT (2.1±0.7) vs. ST (4.7±1.5).
SIGNIFICANCE: The data suggest that BMC promoted a redox status favorable to the oxidation of the pro-inflammatory cytokines in the myocardium, exerting an anti-inflammatory-like effect.
Angela Maria Vicente Tavares; Alex Sander da Rosa Araújo; Guilherme Baldo; Ursula Matte; Neelam Khaper; Adriane Belló-Klein; Luis Eduardo Rohde; Nadine Clausell
Related Documents :
17692407 - G-csf after myocardial infarction accelerates angiogenesis and reduces fibrosis in swine.
12767547 - Electrocardiographic prediction of the development and site of acute myocardial infarct...
24005467 - Coil embolisation of a septal artery in a patient with hypertrophic obstructive cardiom...
18940277 - Differential impact of admission c-reactive protein levels on 28-day mortality risk in ...
15902827 - Coronary thrombosis related to use of xenadrine rfa.
22876297 - Aromatase inhibition attenuates desflurane-induced preconditioning against acute myocar...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-10-21
Journal Detail:
Title:  Life sciences     Volume:  87     ISSN:  1879-0631     ISO Abbreviation:  Life Sci.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-29     Completed Date:  2010-12-22     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0375521     Medline TA:  Life Sci     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  699-706     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Inc. All rights reserved.
Cardiovascular Research Laboratory, Hospital de Clinicas de Porto Alegre, Porto Alegre-RS, Brazil.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Blotting, Western
Bone Marrow Transplantation / methods*
Cytokines / metabolism
Disease Models, Animal
Inflammation / etiology,  therapy*
Interleukin-6 / metabolism
Myocardial Infarction / physiopathology,  therapy*
Myocardium / pathology
Oxidative Stress*
Rats, Wistar
Tumor Necrosis Factor-alpha / metabolism
Reg. No./Substance:
0/Cytokines; 0/Interleukin-6; 0/Tumor Necrosis Factor-alpha

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Bip overexpression, but not CHOP inhibition, attenuates fatty-acid-induced endoplasmic reticulum str...
Next Document:  Investigation of the cardiomyocyte dysfunction in bradykinin type 2 receptor knockout mice.