Aspalathin ameliorates doxorubicin-induced oxidative stress in H9c2 cardiomyoblasts

Aspalathin (ASP) is a C-dihydrochalcone abundantly found in Aspalathus linearis. While we have provide evidence that ASP can protect H9c2 cardiomyoblasts against doxorubicin (Dox)-induced apoptosis through regulation of autophagy, the complete mechanism involved in the cardioprotective effect of this dihydrochalcone remains to be explored. Here we provide evidence that ASP reverses Dox-induced apoptosis through the amelioration of oxidative stress in H9c2 cardiomyoblasts. Cultured cells were treated with 0.2 mu M Dox or co-treated with either 20 mu M dexrazoxane (Dexra) or 0.2 mu M ASP daily for five days, to a final dose of 1 mu M Dox, 100 mu M Dexra and 1 mu M ASP, respectively. Superoxide dismutase, catalase, glutathione, malondialdehyde and dichlorodihydro-fluorescein diacetate fluorescence were used as end-point measurements for oxidative stress, while JC-1 and TUNEL labeling were performed to assess mitochondria depolarization and apoptosis. Co-treatment with ASP attenuated Dox-induced cardiotoxicity by improving endogenous antioxidant levels and mitochondrial membrane potential, while inhibiting reactive oxygen species production and cellular apoptosis. These findings suggested that ASP can prevent Dox-induced oxidative stress and apoptosis and needs further assessment to confirm its therapeutic potential to prevent Dox-induced cardiotoxicity.