Ferulic acid protects against cardiac injury by scavenging
free radicals. However, the role of mitophagy in
ferulic acid-induced cardioprotection remains obscure. In the present study, H9c2 cells were exposed to
hypoxia/reoxygenation and
ferulic acid treatment during
hypoxia. We illustrated the impact of
ferulic acid on oxidative damage in H9c2 cells. Our results showed that
ferulic acid significantly attenuated apoptosis induced by
hypoxia/reoxygenation injury and reduced
mitochondrial dysfunction, evidenced by a decline in the overproduction of
reactive oxygen species and
ATP depletion and recovery of the membrane potential. We also found that mitophagy, a selective form of autophagy, was excessively activated in H9c2 cells subjected to
hypoxia/reoxygenation.
Ferulic acid reduced the binding of mitochondria to lysosomes, down-regulated the PINK1/Parkin pathway, and was accompanied by increased p62 and decreased LC3-II/LC3-I levels.
Ferulic acid also antagonistically reduced the activation of mitophagy by
rapamycin. These findings suggest that
ferulic acid may protect H9c2 cells against
ischemia/reperfusion injury by suppressing PINK1/Parkin-dependent mitophagy. Accordingly, our findings may provide a potential target and powerful reference for
ferulic acid in clinical prevention and treatment of
hypoxia/reoxygenation injury.