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Oxidative stress plays a major part in myocardial reperfusion injury. Cul4a is the core protein of CRLs E3 ubiquitin ligase complex; while it is known that Cul4a is responsible for various cancers, its role in cardiac function remains unclear. Hence, we have shown the protective function of Cul4a and its protection mechanism in oxidative stress-induced H9c2 cardiomyocyte apoptosis. Here, oxidative stress was induced by hydrogen peroxide (H 2 O 2 ), CCK-8 assay and flow cytometry were used to analyze cell viability and apoptosis rate, western blot and immunofluorescence were used to quantitatively analyze the expression of protein, ROS fluorescence kit was used to detect reactive oxygen species (ROS) formation, and coimmunoprecipitation was used to identify protein interaction. In the results, it was found that Cul4a was involved in oxidative stress-induced H9c2 cell apoptosis and could inhibit H 2 O 2 -induced ROS generation and H9c2 cell apoptosis. Furthermore, we identified that when combining with PARP1, Cul4a could reduce its expression, and the interaction was enhanced under oxidative stress. In conclusion, our results indicate that Cul4a is a new protective factor involved in oxidative stress-induced cardiomyocyte injury and functions by tying and decreasing overactivated PARP1.

Cul4a as a New Interaction Protein of PARP1 Inhibits Oxidative Stress-Induced H9c2 Cell Apoptosis