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DOX\u2010induced oxidative damage and cardiomyocyte loss have been recognized as the potential causative mechanisms of this cardiac toxicity. Growing interests are raised on mulberrin (Mul) for its wide spectrum of biological activities, including antioxidative and anti\u2010inflammatory properties. The aim of this study was to investigate the effect of Mul on DOX\u2010induced heart injury and to clarify the underlying mechanism. Mice were given daily 60\u2009mg\/kg of Mul via gavage for 10 days. Mice received an intraperitoneal injection of DOX to mimic the model of DOX\u2010related acute cardiac injury at the seventh day of Mul treatment. Mul\u2010treated mice had an attenuated cardiac injured response and improved cardiac function after DOX injection. DOX\u2010induced oxidative damage, inflammation accumulation, and myocardial apoptosis were largely attenuated by the treatment of Mul. Activated protein kinase B (AKT) activation was essential for the protective effects of Mul against DOX\u2010induced cardiac toxicity, and AKT inactivation abolished Mul\u2010mediated protective effects against DOX cardiotoxicity. In conclusion, Mul treatment attenuated DOX\u2010induced cardiac toxicity via activation of the AKT signaling pathway. Mul might be a promising therapeutic agent against DOX\u2010induced cardiac toxicity.<\/jats:p>","DOI":"10.1155\/2022\/2967142","type":"journal-article","created":{"date-parts":[[2022,7,7]],"date-time":"2022-07-07T23:05:26Z","timestamp":1657235126000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Mulberrin Confers Protection against Doxorubicin\u2010Induced Cardiotoxicity via Regulating AKT Signaling Pathways in 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