The protective mechanism of schisandrin A in d-galactosamine-induced acute liver injury through activation of autophagy.

CONTEXT

The principal bioactive lignan of Schisandra chinensis fructus, commonly used for traditional Chinese medicine, is schisandrin A. Schisandrin A has been widely reported as being very effective for the treatment of liver disease. However, the mechanisms of its protective effects in liver remain unclear.

OBJECTIVE

To explore the hepatoprotective mechanisms of schisandrin A.

MATERIALS AND METHODS

d-Galactosamine (d-GalN)-induced liver injury in mice was used as a model. Schisandrin A was examined for its protective mechanisms using hematoxylin-eosin (HE) staining, enzyme-linked immunosorbent assay (ELISA), western blotting and real-time PCR (RT-PCR).

RESULTS

Aspartate amino-transferase (AST) and alanine transaminase (ALT) levels in the schisandrin A group were significantly decreased (p < 0.01) compared with those in the d-GalN-treated group. HE results showed that the pathological changes in hepatic tissue seen in the d-GalN-treated were reduced in the schisandrin A/d-GalN-treated group, with the morphological characteristics being close to those of the control (untreated) group. Western blotting results showed that schisandrin A can activate autophagy flux and inhibit progression of apoptosis. The immune function of the schisandrin A-pretreated group was assayed by flow cytometry. It was found that the mechanism may involve activated autophagy flux, inhibited apoptosis, and improved immunity in response to liver damage.

CONCLUSION

Our results show that the hepatoprotective mechanisms of schisandrin A may include activation of autophagy flux and inhibition of apoptosis. These results provide pharmacological evidence supporting its future clinical application.