IL-22 ameliorated cardiomyocyte apoptosis in cardiac ischemia/reperfusion injury by blocking mitochondrial membrane potential decrease, inhibiting ROS and cytochrome C.

Abstract Irreversible cardiomyocyte death is one of the main reasons of heart failure following cardiac injury. Therefore, controlling cardiomyocyte death is an effective method to delay the progression of cardiac disease after injury. IL-22 plays critical roles in tissue homeostasis and repair, and has become an important bridge between the immune system and specific tissues or organs. However, whether IL-22 can prevent of cardiomyocyte apoptosis from cardiac injury remains unclear. Therefore, the present work would address the above question. Our results showed that, in vitro, IL-22 prevented cardiomyocyte apoptosis induced by Angiotensin II via enhancing the activity of SOD, blocking the decrease of mitochondrial membrane potential, inhibiting ROS production and release of cytochrome C. The similar results were also found in vivo and patients. Our results shed a light on the therapy of cardiac injury.