{'fraction_non_alphanumeric': 0.02989821882951654, 'fraction_numerical': 0.006997455470737914, 'mean_word_length': 5.665254237288136, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Puerarin protects against myocardial ischemia/reperfusion injury by inhibiting endoplasmic reticulum stress and apoptosis via activating the AMPK/NRF2 pathway


 Objective

Puerarin was reported to protect against myocardial ischemia/reperfusion (IR) injury. The current study aims to investigate the protective effects of puerarin against myocardial IR injury and the underlying mechanisms.
Methods

The hearts were subjected to the ligation of the left anterior descending coronary artery and reperfusion. Before reperfusion, pretreatment with puerarin (100 mg/kg), with or without the AMPK inhibitor Compound c (0.25 mg/kg). Myocardial infarct size, the serum creatine kinase-MB (CK-MB) activity, cardiac function, apoptotic cell death, and the endoplasmic reticulum stress, as well as activation of the AMPK/NRF2 pathway were observed.
Results

Treatment with puerarin significantly decreased the myocardial infarct size, the serum CK-MB activity and notably alleviated IR-induced cardiac dysfunction. Moreover, puerarin reduced myocardial IR-induced apoptotic cell death. In addition, puerarin inhibited myocardial IR-induced endoplasmic reticulum stress and activated the AMPK/NRF2 pathway. More importantly, the AMPK inhibitor Compound c prevented these puerarin-induced cardioprotective effects and activation of the AMPK/NRF2 pathway, as well as apoptosis and the endoplasmic reticulum stress activation.
Conclusion

Our results show that puerarin alleviates myocardial IR injury by inhibiting apoptosis and endoplasmic reticulum stress via the AMPK/NRF2 pathway.