We investigated the protective effect of
Hyperoside (HPS) on liver injury induced by
acetaminophen (
APAP) in C57 mice. HPS was administered orally for 7 days and
APAP was administered orally on the 7th day. Serum and liver samples were then collected for biochemical analyses, histopathology assessments, and metabolomics studies. Metabolites were assessed using a UHPLC-MS system. Principal component analysis (PCA) and orthogonal partial least squares discriminant analysis (OPLS-DA) were used to process the data. Pathway analyses were performed using Metaboanalyst 4.0. Western blot and qRT-PCR were used to determine the
protein and
mRNA levels, respectively. HPS interacted with active sites in
CYP2E1 and caused protein degradation. In conclusion, our results suggested that HPS prevented the oxidative stress-induced liver injury caused by
APAP. PRACTICAL APPLICATIONS:
Hyperoside was shown to have potential protective and
therapeutic effects against
liver diseases. Male C57 mice were used to perform pharmacodynamic, pharmacology, and metabolomics evaluations. At a dose of 60 mg/kg, HPS prevented oxidative stress-induced liver injury caused by
APAP by regulating the
glutathione-related metabolites and
enzymes through the inhibition of
CYP2E1.