Mechanism of Flurbiprofen Axetil Participating in Myocardial Ischemia, Hypoxia and Reperfusion Injury

Aim/Background: The myocardial ischemia, hypoxia and reperfusion injury is the main reason for the aggravation of myocardial injury in acute myocardial infarction. Flurbiprofen axetil has reported to relieve the cerebral ischemia and hypoxia reperfusion injury in rats. Whether flurbiprofen axetil can relieve the myocardial ischemia, hypoxia and reperfusion injury is worthy to be discussed. Methods: CCK-8 assay was to determine the maximum nontoxic dose of flurbiprofen axetil and optical action time for H9c2 cells. The apoptosis of H9c2 cells was detected by flow cytometry analysis. Western blot was to analyze the expression of apoptosis related proteins and TLR4/NF-kappa B signal pathway related proteins. ELISA assay and ROS testing kit were respectively determine the expression of inflammatory factors and ROS. Result: After reperfusion, the apoptosis of H9c2 cells was promoted with the apoptosis-related proteins (Bcl-2, Bax, Cleaved caspase3 and Caspase3) being changed. The inflammatory factors (IL-1, IL-1 beta and COX2) and ROS were significantly increased. OGD/R injury also enhanced the activation of proteins (TLR4, HMGB-1, MYD88 and NF-kbp65) in TLR4/NF-kappa B signal pathway. All these changes were reversed by pretreatment with flurbiprofen axetil to some extent in H9c2 cells. Conclusion: The study indicates that flurbiprofen axetil pre-treatment protects the H9c2 cells from OGD/R injury through reducing apoptosis, inflammation and oxidative stress.