LAUSR

Morin (MO), a natural bioflavinoid, exists in many herbs. Previous studies have acclaimed MO's anti‐inflammatory, antidiabetic, antioxidant, antifibrotic, anticancer, and antihyperglycemic biological effects. This study aimed to assess the molecular mechanism of MO involved in the oleic acid (OA)‐induced inflammatory damage and lipid accumulation in HepG2 cell and tyloxapol (Ty)‐induced hyperlipidemia in mice. We found that MO can efficaciously mitigate reactive tumor necrosis factor‐α (TNF‐α) level and triglyceride (TG) accumulation in OA‐induced HepG2 cell and in tyloxapol‐induced mice. Next, the study testified that MO apparently suppressed OA‐excited nuclear factor‐kappa B (NF‐κB) and mitogen‐activated protein kinases (MAPKs) signaling pathways in HepG2 cell. In addition, MO distinctly upregulated the expression of peroxisome proliferator‐activated receptor α (PPARα) and decreased the expression of sterol regulatory element‐binding protein 1c (SREBP‐1c) in OA‐induced HepG2 cell and in tyloxapol‐induced mice, both of which are dependent upon the phosphorylation of acetyl‐CoA carboxylase (ACC), adenosine 5′‐monophosphate (AMP)‐activated protein kinase (AMPK), and protein kinase B (AKT). In conclusion, these results suggest that MO has protective potential against hyperlipidemia and steatosis, and the potential mechanism may have a close relation with activation of PPARα and inhibition of SREBP‐1c.