Objective: To study the hepatoprotective effects of extracts from processed Corni Fructus against D-galactose-induced liver injury in mice.
Methods: Acute liver injury model was established by D-galactose. The activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD) and level of liver malondialdehyde (MDA) of serum was measured. Hematoxylin and Eosin (HE) staining of pathological section and transmission electron microscopic observation were used to measure the apoptosis of liver cells.
Results: Compared with the normal control group, SOD activity was decreased, MDA level and ALT, AST activity was increased in the model group, and the differences were significant (P < 0.05); While three kinds of cornel active sites showed significant improvement with increasing SOD activity and decreasing ALT, AST activity and MDA levels (P < 0.05). Furthermore, model group appeared obvious necrosis inflammation, and apoptosis characteristics; While liver structural damage were improved significantly in cornel active site groups.
Conclusion: Cornel polysaccharide extract, n-butanol extraction site and petroleum ether extraction sites all have hepatoprotective effects, suggesting that they are the active material of cornel product, and the mechanism may be related to the inhibition of oxidative stress and inflammatory response.