Protective effect of overexpression of PrxII on H2O2-induced cardiomyocyte injury.

Objective: Oxidative stress is one of the main factors leading to myocardial cell damage, and the redox imbalance promotes apoptosis. Therefore, the purpose of this study was to explore the protective effect of PrxII on H2O2-induced H9c2 cell injury.
Materials and Methods: The overexpressed PrxII cell model was constructed by virus. The H9c2 cells were treated with H2O2, and the supernatant and cells were collected. Then, the chymotrypsin-like activity, caspase-like activity, and trypsin-like activity were detected by the kit, and the expressions of P21, P27, and P53 were detected by the ELISA method. Finally, the expressions of antioxidant factors, apoptosis-related factors, and AMPK/Sirt1 signaling pathway were detected by Western blot and Real-time polymerase chain reaction (PCR).
Results: Overexpression of PrxII inhibited the decrease of enzyme activity induced by H2O2, promoted the expressions of anti-oxidation factors GPX1, GPX2, and GSX, and inhibited the expressions of apoptosis-related factors P21, P27, and P53, and activated AMPK/Sirt1 pathway.
Conclusions: Overexpression of PrxII can activate the AMPK/Sirt1 pathway, thereby inhibiting H2O2-induced oxidative stress and slowing apoptosis.