Ozone pretreatment alleviates ischemiareperfusion injury-induced myocardial ferroptosis by activating the Nrf2/Slc7a11/Gpx4 axis.

Myocardial ischemiareperfusion injury (MIRI) is defined as the additional damage that occurs during the process of restoring blood flow to the heart tissue after ischemia-induced damage. Ozone is a powerful oxidizer, but low concentrations of ozone can protect various organs from oxidative stress. Some studies have demonstrated a link between ozone and myocardioprotection, but the mechanism remains unclear.

Ozone treatment alleviates brain injury in cerebral ischemic rats by inhibiting the NF-κB signaling pathway and autophagy.

Stroke is the most frequent cause of disability in developed countries. A common phenomenon of stroke, cerebral ischemia, is threatening many lives worldwide. In addition, ozone treatment was previously reported to exert functions in relieving brain injury.

Ozone induces tolerance against cardiomyocytes oxygen-glucose deprivation/reperfusion through inhibition of autophagy pathway.

Previous studies have reported that excess activation of autophagy in cardiomyocytes is associated with an increase in myocardial oxygen-glucose deprivation/reperfusion (OGD/R) injury. Ozone therapy affords significant cardio-protection against myocardial OGD/R injury. The present study was designed to determine whether ozone-induced tolerance to myocardial OGD/R injury was mediated by inhibiting autophagy.

Ozone Attenuated H9c2 Cell Injury Induced by Doxorubicin.

Doxorubicin (DOX) is a commonly used drug in the treatment of cancers, whereas its application in the clinical stage is restricted because of side effects such as cardiomyocyte injury. Increasing studies indicated that ozone may protect cardiomyocytes from injuries. This study aimed to explore the effects of ozone on cardiotoxicity induced by DOX treatment.