Isoquercetin ameliorated hypoxia/reoxygenation-induced H9C2 cardiomyocyte apoptosis via a mitochondrial-dependent pathway.

Isoquercetin exerts multiple pharmacological effects against various diseases. The present research sought to further investigate the role of isoquercetin in hypoxia/reoxygenation (H/R)-treated cardiomyocytes and its potential mechanism involved. The H/R model in H9C2 cells was established to mimic myocardial I/R injury in vitro. Cell proliferation and apoptosis were tested using MTT assay and Annexin V FITC-PI staining assay, respectively. We found that isoquercetin protected H9C2 cells from H/R-induced injury as the evidences that isoquercetin administration attenuated the effects of H/R treatment on H9C2 cell viability, cell apoptosis and ROS generation after H/R treatment. More importantly, isoquercetin protects mitochondrial function and prevents cytochrome c release in H9C2 cells after I/R injury. In conclusion, these results revealed the potential cardiovascular protective effects of isoquercetin in the treatment of I/R-related myocardial injury.