Bone marrow derived cells decrease inflammation but not oxidative stress in an experimental model of acute myocardial infarction.
OBJECTIVE
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.


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.


RESULTS
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).


CONCLUSIONS
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.
Cardiovascular Research Laboratory, Hospital de Clinicas de Porto Alegre, Porto Alegre-RS, Brazil.
Angela Maria Vicente
AM
Tavares
Alex Sander
AS
da Rosa Araújo
Guilherme
G
Baldo
Ursula
U
Matte
Neelam
N
Khaper
Adriane
A
Belló-Klein
Luis Eduardo
LE
Rohde
Nadine
N
Clausell
D000818:Animals; D015153:Blotting, Western; D016026:Bone Marrow Transplantation / Q000379:methods*; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D004452:Echocardiography; D007249:Inflammation / Q000209:etiology / Q000628:therapy*; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D009203:Myocardial Infarction / Q000503:physiopathology / Q000628:therapy*; D009206:Myocardium / Q000473:pathology; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D013053:Spectrophotometry; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D016207:Cytokines; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha