Aucubin inhibited lipid accumulation and oxidative stress via Nrf2/ HO ‐1 and AMPK signalling pathways

Aucubin ( AU ) is the main active ingredient of Aucuba japonica which has showed many positive effects such as anti‐inflammation and liver protection. Non‐alcoholic fatty liver disease ( NAFLD ) is the most common cause of chronic liver disease. In this research, we explored the effects of AU on the tyloxapol‐induced NAFLD in mice and apolipoprotein C‐ III (apoC‐ III ) induced‐3T3L1 cells. Tyloxapol (300 mg/kg) was injected to C57 BL /6 mice with aucubin. The differentiated 3T3‐L1 cells were treated with or without aucubin after stimulation of apoC‐ III (100 μg/mL). In results, aucubin inhibited hyperlipidaemia, oxidative stress and inflammation by influencing the content of total cholesterol ( TC ), triglyceride ( TG ), low density lipoprotein ( LDL ), very low density lipoprotein ( VLDL ), myeloperoxidase ( MPO ), superoxide dismutase ( SOD ), tumour necrosis factor receptor‐α ( TNF ‐α), interleukin‐1β ( IL ‐1β), and IL ‐6 in blood. AU activated NF ‐E2‐related factor 2 (Nrf2), peroxisome proliferator‐activated receptor α ( PPAR α), PPAR γ and hemeoxygenase‐1 ( HO ‐1) and promoted the phosphorylation of adenosine 5′‐monophosphate‐activated protein kinase ( AMPK α), AMPK β, acetyl‐CoA carboxylase ( ACC ) and protein kinase B ( AKT ). In conclusion, AU performed the function of hypolipidaemic by its obvious anti‐inflammation and antioxidant activity, which may become a kind of new drug targeting at NAFLD .