Use of selective COX-2 non-steroidal anti-inflammatory drugs (NSAIDs) (coxibs) has been associated with an increased risk of acute myocardial infarction (AMI).
Arctigenin treatment also suppressed the protein expression levels of inducible nitric oxide synthase (iNOS), cyclooxygenase 2 (COX‑2) and heme oxygenase 1 (HO‑1), and increased the protein expression levels of phosphorylated‑extracellular signal‑regulated kinase 1/2 (p‑ERK1/2) in AMI rats.
In conclusion, the present study demonstrated that diminazene attenuated AMI in rats via suppression of inflammation, reduction of COX‑2 and iNOS expression, and activation of the ACE2/AT1R/MasR signaling pathway.
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.