Objective    To study the protective effects of nuclear factor-κB inhibitor

pyrrolidine dithiocarbamate (PDTC)

on ventricular dilatation and heart failure induced by experimental myocardial ischemic injury in rats and its mechanisms.     Methods    High dose of isoprenaline (ISO) was used to induce experimental myocardial ischemic injury in rats. Seventy male Wistar rats were divided into three groups: control group (20 rats)

ISO group (30 rats) and ISO+PDTC group (20 rats). Myocardial pathomorphologic changes

NF-κB p65 activation

MCP-1 mRNA expression and serum MCP-1 were investigated. Then ventricular dilatation and left ventricular (LV) function were assessed by echocardiography on day 14 of the experiment.     Results    Myocardial NF-κB was activated

and MCP-1 mRNA expression and serum MCP-1 increased markedly after myocardial ischemic injury induced by ISO (P0.01). PDTC inhibited the activation of myocardial NF-κB and significantly decreased myocardial MCP-1 mRNA expression (P0.01)

serum MCP-1 (P0.01)

myocardial inflammation and injury. On the other hand

PDTC delayed replacement of the damaged myocardium with granulation tissue. On day 14 of the experiment

a marked decrease in left ventricular end-systolic dimension (LVESD) and a significant increase in percentage of ejection fraction were observed in ISO+PDTC group compared with ISO group (P0.05).     Conclusion    The protective effects of PDTC on ventricular dilatation and heart failure may mainly be acquired from the acute stage of heart injury

which mechanisms are probably associated with inhibited activation of myocardial NF-κB

decreased myocardial MCP-1 mRNA expression

serum MCP-1

lessened myocardial inflammation and injury.