Exosomes from Adipose-Derived Mesenchymal Stem Cells Protect Against Cyclophosphamide-Induced Cardiotoxicity in Rats

A certain dosage of cyclophosphamide (CYP) in clinical applications contributes to severe cardiotoxicity. Herein, this study explored the impact of adipose-derived mesenchymal stem cell (AdMSC)-exosomes (Exos) on CYP-induced cardiotoxicity.AdMSCs and AdMSCs-Exos were isolated and identified. CYP was...

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Bibliographic Details
Published inInternational Heart Journal Vol. 64; no. 5; pp. 935 - 944
Main Authors Xiong, Jianhua, Ding, Binjun, Zhu, Wei, Xu, Lanlan, Yu, Songping
Format Journal Article
LanguageEnglish
Published Tokyo International Heart Journal Association 30.09.2023
Japan Science and Technology Agency
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Summary:A certain dosage of cyclophosphamide (CYP) in clinical applications contributes to severe cardiotoxicity. Herein, this study explored the impact of adipose-derived mesenchymal stem cell (AdMSC)-exosomes (Exos) on CYP-induced cardiotoxicity.AdMSCs and AdMSCs-Exos were isolated and identified. CYP was utilized for developing a cardiotoxicity rat model, after which blood was collected and then the serum contents of cardiac injury-related indexes (creatine kinase-MB, lactate dehydrogenase, aspartate aminotransferase, and alkaline phosphatase) were detected with enzyme-linked immunosorbent assay kits. Oxidative stress (OS)-related indicators were measured with the corresponding kits. Myocardial pathological changes and collagen fibrosis were tested with hematoxylin-eosin and Masson staining, and apoptosis-related and autophagy-related proteins in rat cardiac tissues with immunohistochemistry and Western blot assays, respectively.AdMSCs and AdMSCs-Exos were successfully isolated. AdMSCs-Exos could target rat hearts. AdMSCs-Exos improved cardiac function and diminished the content of the cardiac injury-related indexes in CYP rats. In addition, AdMSCs-Exos reduced CYP-induced cardiac fibrosis, OS, apoptosis, and autophagy in rats.AdMSCs-Exos alleviated CYP-induced cardiotoxicity in rats via the repression of OS, apoptosis, and autophagy.
ISSN:1349-2365
1349-3299
DOI:10.1536/ihj.23-201