Cox-2 Negatively Affects the Protective Role of Propofol against HypoxiaReoxygenation Induced Cardiomyocytes Apoptosis through Suppressing Akt Signaling

Abstract EN

Nowadays, the prevention of severe myocardium injury resulting from myocardial ischemia/reperfusion injury (I/R) has been recognized as an important subject in the field of ischemic heart disease.

In this study, H9c2 cardiomyocytes were exposed to cycles of hypoxia/reoxygenation (H/R) to mimic myocardial I/R injury.

Western blot analysis and qRT-PCR were performed to detect the expression of Cox-2, Akt and p-Akt.

Cell viability, LDH release and activity of Caspase-3 were assessed to determine the protective effect of propofol.

The results proved that the protective effect of propofol for H/R challenged cardiomyocytes was associated with Akt phosphorylation.

We also revealed that treatment of propofol suppressed the expression of Cox-2 in cardiomyocytes which was up-regulated after H/R treatment.

Conversely, the over-expression of Cox-2 inhibited Akt phosphorylation while enhancing cardiomyocytes apoptosis.

Interestingly, Akt activator exhibited similar protective effect with propofol and could diminish the influences brought by over-expression of Cox-2.

Thus, it could be concluded that Cox-2 negatively affects the protective effect of propofol against hypoxia/reoxygenation induced cardiomyocyte apoptosis by suppressing Akt phosphorylation.