Polydatin protects against acute myocardial infarction-induced cardiac damage by activation of Nrf2/HO-1 signaling
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Polydatin is a traditional Chinese medicine that provides myocardial protection after acute myocardial infarction (AMI). The study aim was to investigate the myocardial protection polydatin in H9c2 myocardial cells cultured in a hypoxic atmosphere and in a rat AMI model induced by ligating the left anterior descending coronary artery and treated with polydatin 100 mg/kg/day for 30 days. The involvement of Nrf2 in mediating the effects of polydatin was investigated in H9c2 cells following Nrf2 knockdown by transfection of siRNA. Polydatin suppressed hypoxia-induced H9c2 cell apoptosis and reactive oxygen species (ROS) generation by promoting Nrf2/HO-1 signaling. Nrf2 knockdown reversed the protective effects of polydatin against hypoxia-induced myocardial cell injury. The in vivo results were consistent with polydatin suppression of apoptosis and ROS generation in myocardial tissue by promotion of Nrf2/HO-1 signaling. In conclusion, polydatin effectively inhibited hypoxia- and AMI-induced myocardial damage by promotion of Nrf2/HO-1 signaling.
KeywordsNrf2 Polydatin Acute myocardial infarction Apoptosis ROS
Compliance of ethical standards
Conflict of interest
The authors declare no conflict of interest.
All animals were treated following the ethical guidelines of the Guide for the Care and Use of Laboratory Animals. The study was approved by, and conducted following the guidelines, of the Ethics Committee of Pudong New Area Gongli Hospital, Shanghai, China. All surgical procedures were performed under anesthesia, and every effort was made to minimize suffering.
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