Study on the mechanism of antidepressant effect of morinda officinalis oligosaccharides

Objective To investigate the antidepressant effect of morinda officinalis oligosaccharides( MOs) and its possible mechanism.Methods Male Sprague- Dawley( SD) rats were randomly divided into6 groups: normal group,model group,high,moderate and low MOs dose groups( 50,25 and 12. 5 mg · kg- 1· d- 1) and fluoxetine group( 10 mg·kg- 1·d- 1). Except the normal group,the rats in all other groups were given chronic unpredictable stress( CUS) to build the depression animal models. The fluoxetine group and the MOs groups were orally administrated once a day for 14 days. The behavioral status of rats was evluated by forced swimming test( FST) and sucrose preference test( SPT). All the rats were executed 24 h after the last administration,the hippocampal tissue separated and cryopreserved for standby. The protein expression of BDNF、GSK- 3β and synapsins( GluR1、PSD95、Synapsin 1) in the hippocampus of rats were tested by Western- blot. Results After 14 dof daily administration of MOs( 25,50 mg·kg- 1·d- 1) and fluoxetine( 10 mg·kg- 1·d- 1),sucrose preference significantly increased in stressed rats( P 0. 05,P 0. 01,P 0. 01 respectively). Chronic administration of MOs( 50 mg·kg- 1·d- 1) and fluoxetine( 10 mg·kg- 1·d- 1)( P 0. 01) decreased the immobility time significantly. In the hippocampus,the content of BDNF( P 0. 01) 、p- GSK- 3β( P 0. 05) and GluR1、PSD95、Synapsin 1( P 0. 05) protein expression levels of model group were significantly lower than normal group. Chronic administration of MOs( 50 mg·kg- 1·d- 1) increased the protein levels of BDNF( P 0. 05) 、p- GSK- 3β( P 0. 01) and GluR1、PSD95、Synapsin 1( P 0. 05),but no significant differences were measured in the protein levels of the totle GSK- 3β. Conclusion MOs has a prominent therapeutic effect on mice model of chronic stress- induced depression and the underlying mechanisms could involve regulating BDNF signaling pathway and enhancing synaptic plasticity.