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Diallyl trisulfide suppresses doxorubicin‐induced cardiomyocyte apoptosis by inhibiting MAPK/NF‐κB signaling through attenuation of ROS generation

Doxorubicin (Dox) is an effective anticancer agent. However, its effectiveness is limited by its cardiotoxic effects. It has also been reported that the mitogen‐activated protein kinase family and NF‐κB can be activated by Dox treatment. DATS has been shown to be a potent antioxidant with cardioprotective effects. We investigate whether Dox induces cardiac apoptosis through JNK‐ and ERK‐dependent NF‐κB upregulation that can be reduced by DATS treatment.