Abstract Title:

Aspalathin ameliorates doxorubicin-induced oxidative stress in H9c2 cardiomyoblasts.

Abstract Source:

Toxicol In Vitro. 2019 Mar ;55:134-139. Epub 2018 Dec 19. PMID: 30576852

Abstract Author(s):

Samukelisiwe C Shabalala, Phiwayinkosi V Dludla, Christo J F Muller, Xolisa Nxele, Abidemi P Kappo, Johan Louw, Rabia Johnson

Article Affiliation:

Samukelisiwe C Shabalala


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 fluorescencewere 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.

Study Type : In Vitro Study

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