Why the study?
There are no effective approaches to prevent doxorubicin-related cardiac complications, and whether asiatic acid could attenuate doxorubicin-related cardiac injury remains unclear.
Does Asiatic acid prevent doxorubicin-induced cardiotoxicity in mice?
Does Asiatic acid prevent doxorubicin-induced cardiotoxicity in mice?
Asiatic acid demonstrates cardioprotective effects against doxorubicin-induced cardiotoxicity in a preclinical mouse model by reducing oxidative stress and apoptosis through AKT pathway activation.
May justify early-phase human trials of Asiatic acid with doxorubicin; leaves open clinical translation from this mouse model.
The use of doxorubicin (DOX) can result in depression of cardiac function and refractory cardiomyopathy. Currently, there are no effective approaches to prevent DOX-related cardiac complications. Asiatic acid (AA) has been reported to provide cardioprotection against several cardiovascular diseases. However, whether AA could attenuate DOX-related cardiac injury remains unclear. DOX (15 mg/kg) was injected intraperitoneally into the mice to mimic acute cardiac injury, and the mice were given AA (10 mg/kg or 30 mg/kg) for 2 weeks for protection. The data in our study found that AA-treated mice exhibited attenuated cardiac injury and improved cardiac function in response to DOX injection. AA also suppressed myocardial oxidative damage and apoptosis without affecting cardiac inflammation in DOX-treated mice. AA also provided protection in DOX-challenged cardiomyocytes, improved cell viability, and suppressed intracellular reactive oxygen species (ROS) in vitro. Detection of signaling pathways showed that AA activated protein kinase B (AKT) signaling pathway in vivo and in vitro. Furthermore, we found that AA lost its protective effects in the heart with AKT inactivation. In conclusion, our results found that AA could attenuate DOX-induced myocardial oxidative stress and apoptosis via activation of the AKT signaling pathway.
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Li et al. (2020) studied this question.
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