ReferenceID 2143
Mulberrin Confers Protection against Doxorubicin-Induced Cardiotoxicity via Regulating AKT Signaling Pathways in Mice
Oxid Med Cell Longev
Doxorubicin (DOX) is an antitumor anthracycline, but its clinical use was largely limited by its cardiac toxicity. DOX-induced oxidative damage and cardiomyocyte loss have been recognized as the potential causative mecha
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Record Fields
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- Reference Id
- 2143
- Evidence Id
- 18733
- Core Evidence Id
- 18733
- Source Reference Id
- 4329
- Herb2 Reference Id
- HBREF005126
- Subject Paper Key
- HBIN032423_35847586
- Pubmed Id
- 35847586
- Doi
- 10.1155/2022/2967142
- Paper Title
- Mulberrin Confers Protection against Doxorubicin-Induced Cardiotoxicity via Regulating AKT Signaling Pathways in Mice
- Paper Abstract
- Doxorubicin (DOX) is an antitumor anthracycline, but its clinical use was largely limited by its cardiac toxicity. DOX-induced 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-inflammatory properties. The aim of this study was to investigate the effect of Mul on DOX-induced heart injury and to clarify the underlying mechanism. Mice were given daily 60 mg/kg of Mul via gavage for 10 days. Mice received an intraperitoneal injection of DOX to mimic the model of DOX-related acute cardiac injury at the seventh day of Mul treatment. Mul-treated mice had an attenuated cardiac injured response and improved cardiac function after DOX injection. DOX-induced 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-induced cardiac toxicity, and AKT inactivation abolished Mul-mediated protective effects against DOX cardiotoxicity. In conclusion, Mul treatment attenuated DOX-induced cardiac toxicity via activation of the AKT signaling pathway. Mul might be a promising therapeutic agent against DOX-induced cardiac toxicity.
- Journal
- Oxid Med Cell Longev
- Publish Year
- 2022
- Experiment Subject
- mouse
- Experiment Type
- Animal Experiment
- Phenotype Related
- Cardiac Injury; Heart Injury; Cardiac Toxicity
- Paper Title Cn
- Paper Title En
- Mulberrin Confers Protection against Doxorubicin-Induced Cardiotoxicity via Regulating AKT Signaling Pathways in Mice
- Bilingual Status
- semi_complete