Changes in the production of IL-10 and TNF-alpha in skeletal muscle of rats with heart failure secondary to acute myocardial infarction.
BACKGROUND
Recent studies show that the expression of inflammatory mediators, such as cytokines, is an important factor for the development and progression of heart failure (HF), especially in the presence of left ventricular dysfunction. These changes have been demonstrated both in the plasma and heart muscle and, more recently, in skeletal muscle of rats and in patients with HF.


OBJECTIVE
To investigate the production and expression of tumor necrosis factor-alpha (TNF) and interleukin-10 (IL-10) in the soleus and the extensor digitorum longus (EDL) muscles of animals with left ventricular dysfunction after myocardial infarction (MI).


METHODS
We used male Wistar rats that underwent ligation of the left coronary artery without reperfusion. Four weeks after this procedure, the animals underwent echocardiography and were divided into the following experimental groups: sham operated (sham) and IM. They remained under observation for a further period of 8 weeks.


RESULTS
The level of the cytokine TNF-alpha increased by 26.5% (p <0.05), and its gene expression increased 3 times (p <0.01). The level of IL-10 decreased by 38.2% (p <0.05). Both changes occurred only in the soleus muscle, with no change in the EDL. The decrease (36.5%, p <0.05) in the IL-10/TNF-alpha ratio was due to both increased tissue levels of TNF-alpha and decreased tissue levels of IL-10.


CONCLUSIONS
Our results showed significant changes in the IL-10/TNF-alpha ratio, which may have an additive role in the assessment of deterioration and progression of left ventricular dysfunction post-MI. Furthermore, our study suggests that these changes seem to be related to the muscle fiber type.
Lopes
Renato Delacio
RD
Universidade de São Paulo, Brazil.
Batista
Miguel Luiz
ML
Batista Júnior
Miguel Luiz
ML
Rosa
José Cesar
JC
Lira
Fabio Santos de
FS
Martins
Eivor
E
Shimura
Alex Yamashita
AY
Brum
Patrícia Chakur
PC
Lancha
Antonio Herbert
AH
Seelaender
Marília C L
MC
Lopes
Antonio Carlos
AC
D000818:Animals; D004195:Disease Models, Animal; D016753:Interleukin-10 / Q000096:biosynthesis* / Q000235:genetics; D008297:Male; D023421:Models, Animal; D018482:Muscle, Skeletal / Q000378:metabolism*; D009203:Myocardial Infarction / Q000150:complications*; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis* / Q000235:genetics; D018487:Ventricular Dysfunction, Left / Q000378:metabolism*; D016276:Ventricular Function
D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10