Inhibition of PKR protects against H₂O₂-induced injury on neonatal cardiac myocytes by attenuating apoptosis and inflammation.

ABSTRACT: Reactive oxygenation species (ROS) generated from reperfusion results in cardiac injury through apoptosis and inflammation, while PKR has the ability to promote apoptosis and inflammation. The aim of the study was to investigate whether PKR is involved in hydrogen peroxide (H₂O₂) induced neonatal cardiac myocytes (NCM) injury. In our study, NCM, when exposed to H₂O₂, resulted in persistent activation of PKR due to NCM endogenous RNA. Inhibition of PKR by 2-aminopurine (2-AP) or siRNA protected against H₂O₂ induced apoptosis and injury. To elucidate the mechanism, we revealed that inhibition of PKR alleviated H₂O₂ induced apoptosis companied by decreased caspase3/7 activity, BAX and caspase-3 expression.

SUBMITTER: Wang Y 

PROVIDER: S-EPMC5144063 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature