To investigate the effect and underlying mechanism of
aescin on acute liver injury induced by
endotoxin, liver injury was established by injecting
lipopolysaccharide (LPS) in mice. Animals were assigned to seven groups: the control group and groups treated with LPS (40 mg/kg),
aescin (3.6 mg/kg), LPS plus
dexamethasone (4 mg/kg) and LPS plus
aescin (0.9, 1.8 or 3.6 mg/kg). Hepatic histopathological changes were examined under a light microscope. Activities of
alanine aminotransferase (ALT) and
aspartate aminotransferase (AST) in serum were determined. Levels of
tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β),
nitric oxide (NO) and antioxidative parameters in liver homogenate were measured.
Glucocorticoid receptor (GR),
11 beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1) and
11 beta-hydroxysteroid dehydrogenase type 2 (11β-HSD2) expressions in liver were determined by western blotting. Treatment with
escin could inhibit immigration of inflammatory cells, alleviate the degree of
necrosis, and decrease serum ALT and AST activities.
Aescin also down-regulated levels of
inflammation mediators (TNF-α, IL-1β and NO) and 11β-HSD2 expression in liver, up-regulated GR expression, enhanced endogenous antioxidative capacity, but have no obvious effect on 11β-HSD1 expression in liver. The findings suggest
aescin has protective effects on
endotoxin-induced liver injury, and the underlying mechanisms were associated with its anti-inflammatory effects, up-regulating GR expression, down-regulating 11β-HSD2 experssion, and antixoidation.