The antioxidant activity and protective effect of quercetin from seabuckthorn meal were studied
in vitro. The antioxidant activities of quercetin in seabuckthorn were studied by 1, 1-diphenyl-2-trinitrophenylhydrazine (DPPH·) superoxide anion (
\rmO_2^- \cdot ), 2, 2-diazo-bis (3-ethyl-benzothiazole-6-sulfonic acid) diammonium salt (ABTS
+·) and high iron ion reduction (FRAP). The aging model of mice was established by subcutaneous injection of D-galactose into the neck. The mice were treated with quercetin of seabuckthorn meal at different doses (100, 250, 500 mg/kg) by gavage. The eyeball blood was taken to measure the activities of total antioxidant capacity (T-AOC), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and malondialdehyde (MDA) in serum; the heart, kidney and liver were taken as hematoxylin eosin staining (HE) to observe the pathological state of the cells. The results showed that quercetin from seabuckthorn meal had good scavenging ability on DPPH·,
\rmO_2^- \cdot and ABTS
+·. Compared with the model group, the content of MDA in the low dose group of quercetin of seabuckthorn meal decreased significantly (
P<0.05), the activities of T-AOC, GSH-Px and SOD in the serum of mice in the medium and high dose groups increased significantly (
P<0.05), and the content of MDA decreased significantly (
P<0.05). From the pathological section, with the increase of quercetin dosage in seabuckthorn meal, the myocardial fibers arranged orderly and the transverse lines were clear; the morphology of renal sacs and glomeruli gradually became normal, the number of renal tubules increased and arranged closely; the number of hepatocytes increased, the cell morphology was complete, and the sinus space gradually became significant. Therefore, quercetin from seabuckthorn meal could improve the activity of antioxidant enzymes and the content of reducing substances in aging model mice, reduce the content of lipid peroxide, so as to improve the antioxidant capacity of aging model mice, and had a better protective effect on aging model mice.