Relationship between serum nuclear factor-κB and serum inflammatory cytokines levels in heart failure following acute myocardial infarction in rats

AIM:To study the relationship of serum nuclear factor-κB (NF-κB) and the level of serum TNF-α and high-sensitivity C-reactive protein (hsCRP) in heart failure following acute myocardial infarction (MI) in rats. METHODS: A total of 50 SD rats were randomized into three groups: heart failure group (n=20), treatment group (n=20) and sham-operated group (n=10). Heart failure model was created in rats by coronary artery ligation after MI. After ligation, NF-κB inhibitor pyrrolidine dithiocarbamate was given in drinking water in treatment group and the same amount of distilled water was given in heart failure group and sham-operated group. All surviving models were sacrificed after 6 weeks. Hemodynamic parameters and ventricular mass index were measured. Serum NF-κB and TNF-α levels were detected using ELISA and hsCRP was detected using latex-enhanced immunoturbidimetric assay transmission. RESULTS: Compared with sham-operated group, ventricular remodeling index and lung index in heart failure group and treatment group significantly increased (P<0.05). Compared with heart failure group, indexes in treatment group decreased but were still significantly higher than in sham-operated group (P<0.05). Hemodynamic status significantly decreased in heart failure group and treatment group compared with sham-operated group (P<0.05) and status in the treatment group was superior to that in the heart failure group (P<0.05). Serum NF-κB, TNF-α and hsCRP levels in heart failure group and treatment group significantly increased compared with sham-operated group (P<0.05). Levels in treatment group significantly decreased compared with heart failure group (P<0.05). NF-κB levels were positively correlated with levels of TNF-α (r=0.465, P<0.05) and levels of hsCRP (r=0.323, P<0.05). CONCLUSION: Levels of serum NF-κB and serum TNF-α and hsCRP in heart failure following acute MI in rats increased, suggesting that NF-κB upregulates the levels of inflammatory cytokines in heart failure rats.