Camel Milk Exosomes Alleviate Doxorubicin-Induced Cardiotoxicity by Regulating Apoptosis and Autophagy via the NF-κB and MAPK Pathways

Abstract

Simple Summary Doxorubicin (Dox)-induced cardiotoxicity (DIC) is a major obstacle in cancer treatment. Although camel milk exosomes (CMEs) have several pharmacological effects, their function in DIC remains unclear. By establishing Dox-induced C57BL/6 mice and H9c2 cell injury models, we found that CMEs exert a cardiac protective effect by alleviating oxidative stress and cardiomyocyte apoptosis and regulating autophagy via inhibition of the NF-κB and MAPK signaling pathways.