We suggest that a mulberry anthocyanin extract regulates glucose metabolism by activating the PI3K/AKT pathway in HepG2 cells.

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 Caenorhabditis elegans. 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‐1α that were involved in oxidative stress and insulin signalling modulation. In vivo, extended lifespan was observed in C. elegans damaged by paraquat in the presence of MAE, while these beneficial effects were disappeared in pmk-1 and daf-16 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 C. elegans that suffered from oxidative stress, which might be by targeting MAPKs and Nrf2.

Bayberry-derived cyanidin-3-O-glucoside administration could effectively alleviate the inflammatory response induced by microplastic polystyrene in C57BL/6 mice via promoting the fecal PS discharge and modulating the PS-associated gut microbiome perturbations.