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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 μM Dox or co-treated with either 20 μM dexrazoxane (Dexra) or 0.2 μM ASP daily for five days, to a final dose of 1 μM Dox, 100 μM Dexra and 1 μM ASP, respectively. Superoxide dismutase, catalase, glutathione, malondialdehyde and dichloro-dihydro-fluorescein diacetate fluorescence were used as end-point measurements for oxidative stress, while JC-1 and TUNEL labeling were …