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The rats were subjected to left anterior descending ligation and perfusion surgery. In vitro experiments were performed on H9c2 cells using the oxygen\u2010glucose deprivation\/reoxygenation (OGD\/R) model. The results showed the administration of C3G reduced the infarction area, mitigated pathological alterations, inhibited ST segment elevation, and attenuated oxidative stress and ferroptosis\u2010related protein expression. C3G also suppressed the expressions of USP19, Beclin1, NCOA4, and LC3II\/LC3I. In addition, treatment with C3G relieved oxidative stress, downregulated LC3II\/LC3I, reduced autophagosome number, downregulated TfR1 expression, and upregulated the expressions of FTH1 and GPX4 in OGD\/R\u2010induced H9c2 cells. C3G could inhibit the protein levels of USP19 and LC3II. C3G promoted K11\u2010linked ubiquitination of Beclin1. Further evidence that C3G reduced ferroptosis and ameliorated myocardial I\/R injury was demonstrated with the ferroptosis promoter RSL3. 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