{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["16(3)"],"submitter":["Junhong K"],"pubmed_abstract":["<h4>Aim</h4>(-)-Epicatechin (EPI) has physiological activities such as antioxidant, anti-inflammatory and immune enhancement. In this study, we elucidated the protective effects of EPI in myocardial ischemia/reperfusion injury (MI/RI) and its mechanisms.<h4>Methods</h4>An <i>in vivo</i> I/R model was constructed by performing left anterior descending coronary artery surgery on rats, and an <i>in vitro</i> I/R model was constructed by subjecting hypoxia/reperfusion treatment on H9C2 cells. The damage of cardiac tissues was detected by 2,3,5-triphenyltetrazolium chloride (TTC) and hematoxylin-eosin (H&E) staining, and expressions of ferroptosis-related proteins were examined by Western blot. Changes in the number of autophagosomes, the levels of oxidative stress and Fe<sup>2+</sup> were also examined.<h4>Results</h4>EPI reduced abnormal electrocardiogram waveform and infarct size caused by MI/RI in rats. The increasing trend of levels of reactive oxygen species (ROS) and Fe<sup>2+</sup> was reversed by EPI, suggesting that EPI can reduce ferroptosis <i>in vivo</i>. Moreover, the levels of lipid ROS and LC3 in H9C2 cells were decreased with EPI treatment, and autophagy and ferroptosis were also alleviated in a dose-dependent manner <i>in vitro</i>. Co-cultivation of USP14 inhibitor IU1 and EPI further revealed that EPI regulates ferroptosis through the USP14-autophagy pathway.<h4>Conclusions</h4>EPI can reduce the level of oxidative stress by promoting USP14 to reduce autophagy, thus inhibiting autophagy dependent ferroptosis and reducing oxidative stress, and has a protective effect on myocardial infarction/myocardial infarction."],"journal":["Aging"],"pagination":["2181-2193"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10911377"],"repository":["biostudies-literature"],"pubmed_title":["(-)-Epicatechin protects against myocardial ischemia/reperfusion injury via autophagy-dependent ferroptosis."],"pmcid":["PMC10911377"],"pubmed_authors":["Qian X","Haowen Z","Yuhan D","Junhong K","Guangxing S","Yun T"],"additional_accession":[]},"is_claimable":false,"name":"(-)-Epicatechin protects against myocardial ischemia/reperfusion injury via autophagy-dependent ferroptosis.","description":"<h4>Aim</h4>(-)-Epicatechin (EPI) has physiological activities such as antioxidant, anti-inflammatory and immune enhancement. In this study, we elucidated the protective effects of EPI in myocardial ischemia/reperfusion injury (MI/RI) and its mechanisms.<h4>Methods</h4>An <i>in vivo</i> I/R model was constructed by performing left anterior descending coronary artery surgery on rats, and an <i>in vitro</i> I/R model was constructed by subjecting hypoxia/reperfusion treatment on H9C2 cells. The damage of cardiac tissues was detected by 2,3,5-triphenyltetrazolium chloride (TTC) and hematoxylin-eosin (H&E) staining, and expressions of ferroptosis-related proteins were examined by Western blot. Changes in the number of autophagosomes, the levels of oxidative stress and Fe<sup>2+</sup> were also examined.<h4>Results</h4>EPI reduced abnormal electrocardiogram waveform and infarct size caused by MI/RI in rats. The increasing trend of levels of reactive oxygen species (ROS) and Fe<sup>2+</sup> was reversed by EPI, suggesting that EPI can reduce ferroptosis <i>in vivo</i>. Moreover, the levels of lipid ROS and LC3 in H9C2 cells were decreased with EPI treatment, and autophagy and ferroptosis were also alleviated in a dose-dependent manner <i>in vitro</i>. Co-cultivation of USP14 inhibitor IU1 and EPI further revealed that EPI regulates ferroptosis through the USP14-autophagy pathway.<h4>Conclusions</h4>EPI can reduce the level of oxidative stress by promoting USP14 to reduce autophagy, thus inhibiting autophagy dependent ferroptosis and reducing oxidative stress, and has a protective effect on myocardial infarction/myocardial infarction.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jan","modification":"2025-04-05T11:38:29.077Z","creation":"2025-04-05T11:38:29.077Z"},"accession":"S-EPMC10911377","cross_references":{"pubmed":["38277217"],"doi":["10.18632/aging.205477"]}}