To compare the alleviative effects of native and fermented white ginseng, red ginseng, black ginseng and ginseng berry on exercise-induced fatigue and oxidative damage in mice.

Male Institute of Cancer Research (ICR) mice were assigned to 10 groups of 12 animals each: blank control, positive control (powder in rhodiola capsule), and native and fermented white ginseng, red ginseng, black ginseng and ginseng berry (0.5 g/(kg m_b·d)). The animals in the experimental groups were administered for 30 straight days. Body mass and food intake were recorded. Serum urea nitrogen and serum and muscle lactic acid levels were measured, and the changes in blood glucose levels, the levels of glycogen in muscle and liver and the expression levels of glutathione peroxidase (GSH-Px), total superoxide dismutase and malondialdehyde (MDA) in liver were analyzed. The correlation between anti-fatigue and antioxidant indexes was analyzed.

Body mass increased with administration time for all experimental groups. After 30 days of administration, no significant difference in body mass gain or food intake changes was found among all groups. Compared with the blank control group, the positive control group had a strong protective effect on oxidative damage induced by fatigue stress. Comparison with the positive group, intervention with fermented black ginseng significantly prolonged the exhaustive swimming time of mice (P < 0.01), reduced the levels of blood lactic acid, serum urea nitrogen and muscle lactic acid (P < 0.01), increased the levels of blood glucose, liver glycogen and muscle glycogen (P < 0.05) and the activity of GSH-Px (P < 0.01), and decreased the content of MDA in the liver (P < 0.01).

Fermented black ginseng reduces or eliminates oxidative damage induced by fatigue stress and protects against oxidative stress and exercise fatigue, and its anti-fatigue and antioxidant effects are more pronounced than those of the other ginseng products and powder in rhodiola capsule at the same dose.

To explore the protective effect of arctigenin (ATG) on liver injury in diabetic mice.

Alloxan was used to induce diabetes in male ICR mice. Six groups of mice were set up: control, model, positive control (metformin, Met), and high-, medium-, and low-dose ATG (120, 90 and 60 mg/kg m_b). The activities of alanine aminotransferase (ALT) and asparate aminotransferase (AST) and the concentrations of the inflammatory cytokine interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were in the serum determined. Liver glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD) levels were analyzed, and histomorphological observation of the liver was performed after hematoxylin and eosin staining. Protein expression levels involved in the toll-like receptors (TLR4), myeloid differentiation factor 88 (MyD88) and nuclear factor κB p65 (NF-κB p65) signaling pathways were measured.

Compared with the model group, highdose ATG significantly reduced ALT and AST activities in the serum of diabetic mice (P < 0.01); high- and medium-dose ATG significantly reduced serum IL-6 and TNF-α levels (P < 0.01); high-dose ATG significantly increased liver CAT and SOD activities (P < 0.01) as well as GSH levels (P < 0.05); high- and medium-dose ATG significantly improved the cellular morphology of liver tissue, increasing the red-stained area of cells in liver slices and reducing cell vacuoles and bleeding areas. High-dose ATG significantly reduced the protein expression of TLR4, MyD88 and NF-κB p65 in the liver (P < 0.01 and P < 0.05). The hepatoprotective mechanism of ATG may be related to reducing the expression of key proteins in the TLR4, MyD88 and NF-κB p65 signaling pathways, and inhibiting the expression of downstream inflammatory factors, such as NF-κB, TNF-α and IL-6, thereby reducing the level of oxidative stress.

ATG has a protective effect on diabetic liver injury. This study provides a reference for the application of ATG in the prevention and treatment of diabetic liver injury.