Mulberry Anthocyanin Extract Ameliorates Oxidative Damage in HepG2 Cells and Prolongs the Lifespan of <i>Caenorhabditis elegans</i> through MAPK and Nrf2 Pathways

Abstract

Mulberry anthocyanins possess many pharmacological effects including liver protection, anti-inflammation, and anticancer. The aim of this study was to evaluate whether mulberry anthocyanin extract (MAE) exerts beneficial effects against oxidative stress damage in HepG2 cells and <i>Caenorhabditis elegans.</i> In vitro, MAE prevented cytotoxicity, increased glucose consumption and uptake, and eliminated excessive intracellular free radicals in H₂O₂-induced cells. Moreover, MAE pretreatment maintained Nrf2, HO-1, and p38 MAPK stimulation and abolished upregulation of p-JNK, FOXO1, and PGC-1<i>α</i> that were involved in oxidative stress and insulin signalling modulation. In vivo, extended lifespan was observed in <i>C. elegans</i> damaged by paraquat in the presence of MAE, while these beneficial effects were disappeared in <i>pmk-1</i> and <i>daf-16</i> mutants. PMK-1 and SKN-1 were activated after exposure to paraquat and MAE suppressed PMK-1 activation but enhanced SKN-1 stimulation. Our findings suggested that MAE recovered redox status in HepG2 cells and <i>C. elegans</i> that suffered from oxidative stress, which might be by targeting MAPKs and Nrf2.