Emodin alleviates acute hypoxia-induced apoptosis in gibel carp (Carassius gibelio) by upregulating autophagy through modulation of the AMPK/mTOR pathway

Previous studies have shown that emodin (EMO) has a wide range of pharmacological activities, with the potential to protect against a variety of diseases. However, it is not clear whether EMO can alleviate impairment induced by acute hypoxia in gibel carp. Thus, an acute hypoxia experiment was conducted using gibel carp fed with EMO diets for eight weeks. The results showed that EMO decreased hypoxia signaling by down-regulating protein levels of hypoxia-inducible factor (HIF-1α). This also protected the liver from oxidative damage induced by acute hypoxia, as indicated by the upregulation of mRNA levels and antioxidant enzyme activity of genes related to nuclear factor erythroid 2-related factor 2 (Nrf2) signaling. Moreover, EMO also inhibited endoplasmic reticulum (ER) stress in the liver and hypothalamus induced by acute hypoxia. EMO enhanced autophagy and inhibited apoptosis in gibel carp by mediating the AMPK/mTOR signaling pathway. Overall, EMO could alleviate impairment in gibel carp induced by acute hypoxia via the AMPK/mTOR pathway. • Acute hypoxia induced oxidative stress, ER stress and apoptosis in gibel carp. • EMO decreased hypoxia signaling by down-regulating protein levels of HIF-1α. • EMO improved antioxidant defense as well as inhibited ER stress effects. • Autophagy and inhibited apoptosis was enhanced by EMO in gibel carp. • EMO exerts protective effects by regulating Nrf2/Keap1 and AMPK/mTOR pathways.