Protective effect of diethylcarbamazine inhibits NF-κB activation in isoproterenol-induced acute myocardial infarction rat model through the PARP pathway

The present study investigated the protective effect of diethylcarbamazine in inhibiting nuclear factor (NF)-kappa B activation in isoproterenol-induced acute myocardial infarction (AMI) rats through the poly ADP ribose polymerase (PARP) pathway. Male albino Wistar rats were injected subcutaneously with isoproterenol (100 mg/kg/day) for 2 days to induce an AMI model. Diethylcarbamazine (50 mg/kg) was administered by gavage for 12 days prior to the isoproterenol-induced AMI. It was noted that diethylcarbamazine significantly inhibited AMI-induced casein kinase and lactate dehydrogenase levels, and reduced the AMI-induced wet heart weight to body weight ratio in AMI rats. Diethylcarbamazine treatment significantly weakened reactive oxygen species production and reduced the levels of tumor necrosis factor (TNF)-alpha, interleukin-6 and NF-kappa B/p65 in AMI rats. Western blotting demonstrated that diethylcarbamazine significantly suppressed the AMI-induced inducible nitric oxide synthase (iNOS), transforming growth factor (TGF)-beta 1, cyclooxygenase-2 (COX-2) and PARP protein expression in AMI rats. The results demonstrated that the protective effect of diethylcarbamazine inhibited isoproterenol-induced AMI through the suppression of inflammation, iNOS, TGF-beta 1, COX-2 and the PARP pathway, and revealed the clinical potential of diethylcarbamazine for therapeutic and clinical applications.