Objective To study protective effect and mechanism of bergenin on D-galactosamine (D-GalN)-induced acute liver injury in rats.
Methods Totally 60 Sprague-Dawley (SD) rats were randomly assigned into 6 groups (10 in each group): a control and a model group with saline, a silymarin group (120 mg/kg), and low, moderate and high bergenin groups (20, 40, 80 mg/kg). All the treatments were carried out by intragastric administration (10 mL/kg) once a day consecutively for 7 days. Two hours after the last administration, D-GalN (700 mg/kg) was intraperitoneally administered for all the rats to establish acute liver injury model, excepted for the control rats. Sixteen hours after the D-GalN injections, all rats′ blood and liver tissue specimens were collected. Biochemical methods were used to detect serum content or activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total antioxidant capacity (T-AOC), total bilirubin (TBIL), total superoxide dismutase (T-SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH-Px); enzyme-linked immunosorbent assay (ELISA) was adopted to measure contents of interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in liver tissues; and Western blot analysis was performed to determine phosphorylated c-Jun N-terminal kinase (p-JNK), JNK, c-Jun, phospharylated adenosine monophosphate-activated protein kinase (p-AMPK), and AMPK protein expressions in liver tissues, respectively. Pathological changes of liver tissues were observed with hematoxillin-eosin (HE) staining.
Results Compared with those in the control rats, serum activity of AST, ALT, TBIL and MDA were significantly increased in the model rats (all P < 0.01). In contrast to those in the model rats, serum AST, ALT, TBIL, and MDA were significantly reduced in the rats of the three bergenin groups (all P < 0.05) and the activity of serum T-AOC, T-SOD, and GSH-Px were significantly increased in the rats of moderate and high bergenin groups (all P < 0.01); in addition, significantly decreased TNF-α, IL-1β, IL-6 and increased IFN-γ (all P < 0.01), down-regulated p-JNK and c-Jun expressions (both P < 0.05) but up-regulated p-AMPK expression (P < 0.01) were detected in liver tissues of the rats of moderate and high bergenin groups.
Conclusion Bergenin possesses a protective effect on D-GalN-induced acute liver injury in rats and the mechanism of the effect may be related to the inhibition of oxidative stress and the regulation of AMPK/JNK signaling pathway.
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