| Objectives: The heart failure (HF) represents the final common pathway in the cardiovascular disease. Ventricular remodeling after acute myocardial infarction(AMI) is a changing process of ventricular size, shape, structure and function,which can lead to heart failure. There is increasing evidence that inflammatory cytokines play an important role in the development of heart failure. Nuclear factor–κB is an inflammatory transcription factor, which play an important role in the pathogenesis of heart failure.The activation of inflammatory cytokines(for example, TNF-αor hsCRP) plays an important role in the pathogenesis of HF, it can depressed left ventricular contractility as well as diastolic, inducing cardiac remolding, leading or worsen heart failure. Through establish rat heart failure model using ligation of the left descending anterior coronary, studied the relationship of serum NF-κB and the level of serum TNF-α, hsCRP in heart failure following acute myocardial infarction in rats, investigated the reciprocity of the three factors, the ventricular remoldeling and cardiac function, and observed the expression of NF-κB by the intervention of PDTC in rats with heart failure. This study would provide a new method to retard the process of heart failure.Methods: A total of 50 SD rats were randomized into three groups:①heart failure group(n = 20),②treatment group(n = 20) and③sham-operation group(n = 10). Heart failure model was created in rats by coronary artery ligation after myocardial infarction. After ligation surgery, NF-κB inhibitor pyrrolidine dithiocarbamate was given in drinking water in treatment group and only the amout of distilled water was given in heart failure group and sham-operation group. All the surviving models were sacrificed after 6 weeks.Hemodynamic parameters and ventricular mass index were measured, serum NF-κB and TNF-αlevels were detected using enzyme linked immonosorbant assay and hsCRP was detected using latex enhanced immunoturbidimetric assay transmission.Results:(1) Ventricular remodeling index analysis: Compared with those in sham-operation group, ventricular remodeling 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 those in sham-operation group (P < 0.05).(2) Hemodynamic parameters analysis: There were significantly differences in the left venricular haemogynamics among three groups. The hemodynamic state significantly decreased in heart failure group and treatment group compared with that in sham-operation group(P < 0.05), and the state in treatment group was much better than that in heart failure group(P < 0.05).(3) The serum NF-κB,TNF-αand hsCRP levels in heart failure group and treatment group significantly increased compared with those in sham-operation group(P < 0.05) , and the levels in treatment group significantly decreased compared with those in heart failure group(P < 0.05).(4) The level of NF-κB,TNF-αand hsCRP presented obviously positive correlation with left ventricular end-diastolic pressure (LVEDP) (r = 0.650, P < 0.05; r = 0.659, P < 0.05; r = 0.224, P < 0.05, respectively), and those presented obviously negative correlation with left ventricular pressure maximal rate of rise or fall (r = -0.626, P < 0.05 and r = -0.661, P < 0.05; r = -0.574, P < 0.05 and r = -0.558, P < 0.05; r = -0.339, P < 0.05 and r = -0.334, P < 0.05, respectively).(5) NF-κB levels were positively correlated with the levels of TNF-α(r = 0.465, P < 0.05) and the levels of hsCRP(r = 0.323, P < 0.05).Conclusion:(1) There is heart failure model after myocardial infarction including ventricular remodeling and lung index.(2) The hemodynamic state was significantly declined in heart failure model after myocardial infarction.(3) The levels of serum NF-κB and serum TNF-αand hsCRP in heart failure following myocardial infarction in rats are increased, which are correlated positively with deteriorated cardiac function, and NF-κB might play an important role in the process of heart failure,which upregulates the levels of inflammatory cytokines in heart failure rats.(4) PDTC can reduce the levels of serum TNF-αand hsCRP in heart failure by inhibiting the activity of NF-κB in heart failure, and thus improve the cardiac function.
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