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Measurements of cardiac function, biochemical analysis, and histopathological examinations were conducted to evaluate the therapeutic effects of salidroside. In this study, we found that diabetic mice exhibited decreased cardiac systolic function and impaired mitochondrial ultrastructure. Pre\u2010treatment with salidroside protected mice against myocardial dysfunction, reduced blood glucose, improved insulin resistance, and induced mitochondrial biogenesis. Neonatal rat cardiomyocytes were cultured to explore the mechanisms of salidroside in vitro. Salidroside alleviated decreased expression of peroxisome proliferator\u2010activated receptor\u2010\u03b3 coactivator 1\u2010alpha (PGC\u20101\u03b1), mitochondrial transcription factor A (TFAM) via phosphorylation of 5\u2032 AMP\u2010activated protein kinase (AMPK), which may be associated with mitochondrial biogenesis. Salidroside also increased sirtuin\u20103 (SIRT3) expression in cardiomyocytes. Furthermore, salidroside promoted the translocation of SIRT3 from cytoplasm to mitochondria and increased the deacetylation of mitochondrial proteins such as manganese\u2010dependent superoxide dismutase (MnSOD). In Conclusion, salidroside not only improved diabetes, but also ameliorated diabetic cardiomyopathy, which was at least partly associated with the activation of mitochondrial SIRT3, AMPK\/Akt, and PGC\u20101\u03b1\/TFAM and subsequent improving mitochondrial function.<\/jats:p>","DOI":"10.1002\/ptr.7175","type":"journal-article","created":{"date-parts":[[2021,5,30]],"date-time":"2021-05-30T20:50:22Z","timestamp":1622407822000},"page":"4579-4591","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":53,"title":["Salidroside protects cardiac function in mice with diabetic cardiomyopathy via activation of mitochondrial biogenesis and\n                    <scp>SIRT3<\/scp>"],"prefix":"10.1002","volume":"35","author":[{"given":"Ye","family":"Li","sequence":"first","affiliation":[{"name":"Hubei Key Laboratory of Drug Target Research and Pharmacodynamic Evaluation, Department of Pharmacology, School of Basic Medicine Tongji Medical 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