Ginsenoside Rd ameliorates aflatoxin B1 induced apoptosis via governing antioxidative activity in H9C2 cells and 3D heart spheroids

Abstract

Aflatoxin B1 exerts potent toxic effects on a variety of tissues or organs in the body; it often contaminates the environment and foods, and thus poses a heavy burden on public health and food safety efforts. As an essential botanical medicine, Ginsenoside Rd has been demonstrated to alleviate multiple organ injuries induced by a variety of toxins. Our study aimed to examine how AFB1 influenced heart cell apoptosis in vitro and determine regulatory effects of Rd in the effects of AFB1 on heart function. For this purpose, the H9C2 cell line and 3D primary heart spheroids were used. RT-qPCR was used to measure apoptosis-related genes’ expression levels. siRNA-based gene knockdown was used for mechanistic analyses. The results revealed that AFB1 potently promoted apoptosis-related genes’ (such as caspase-3/9 genes) expression levels in both H9C2 cells and 3D heart spheroids. Rd alleviated AFB1-induced heart cell apoptosis. Oxidative stress induced by H2O2 potently induced heart cell apoptosis. Rd also significantly reduced superoxide dismutase activity in heart spheroids. Finally, it was suggested that attenuation of Rd against AFB1-caused apoptosis of heart cells were mediated through the induction of antioxidant activity. On the whole, the present study provides useful information which may aid in the development of novel antidotes against toxins and their negative effects, including AFB1-induced heart injury.