Abstract:
:The present study investigated the protective effect of diethylcarbamazine in inhibiting nuclear factor (NF)-κB 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)‑α, interleukin‑6 and NF‑κB/p65 in AMI rats. Western blotting demonstrated that diethylcarbamazine significantly suppressed the AMI‑induced inducible nitric oxide synthase (iNOS), transforming growth factor (TGF)‑β1, 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‑β1, COX‑2 and the PARP pathway, and revealed the clinical potential of diethylcarbamazine for therapeutic and clinical applications.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Jia G,Zao M,Liu Xdoi
10.3892/mmr.2017.6695subject
Has Abstractpub_date
2017-08-01 00:00:00pages
1596-1602issue
2eissn
1791-2997issn
1791-3004journal_volume
16pub_type
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