Emodin: Its effects are largely due to hormesis

This present paper provides the first integrative evaluation of the occurrence of emodin-induced hormetic-biphasic dose responses in the biological and biomedical literature, their study design and dose-response features, underlying adaptive and toxic mechanistic foundations, and generality across biological models, cell types, as well as across different levels of biological organization (i.e., cell, organ, and organism). Emodin-induced hormetic responses have been reported in numerous cellular experimental systems of broad biomedical interest, as well as in in vivo studies with fish and rodent models. Of particular interest was the generality of the in vivo findings across multiple commercial fish models, in which emodin enhanced growth and development and increased resistance to various physical and environmental stressors. While emodin induces hormetic effects via multiple molecular targets and pathways, a general mechanistic adaptive response strategy involves its capacity to activate peroxisome proliferator-activated receptor gamma and the AMPK/Nrf2 pathway.