Apoptosis is mediated by cytosolic phospholipase A2 during simulated ischaemia/reperfusion-induced injury in neonatal cardiac myocytes

It has become increasingly clear that apoptosis plays a major role in ischaemia/reperfusion (I/R)-induced cell death, but the molecular basis of this process remains to be elucidated. Therefore, the aim of this study was to investigate the role of cPLA2 in MAPK phosphorylation and apoptosis in simulated ischaemia/reperfusion (SI/R)-induced injury in neonatal cardiomyocytes. Inhibition of cPLA2 with AACOCF3 significantly improved cell viability during SI/R (60.17±1.77 to 80.17±1.97%, p<0.05). The increase in cell viability was associated with a significant inhibition of p38 phosphorylation (135.3±4.47% to 87.94±10.71%, p<0.001) as well as with a significant decrease in caspase-3- (320.32±17.32% to 146.7±28.69%, p<0.01) and PARP-(263.9±8.15% to 154.7±2.24%, p<0.001) cleavage during SI/R. This study provides evidence for a role for cPLA2 during SI/R-induced injury. It appears that p38 MAPK is a central role player in the signalling pathway involved.