CUMS-induced Mice Research Articles

Extract of sesame cake and sesamol alleviate chronic unpredictable mild stress-induced depressive-like behaviors and memory deficits

Depression is a worldwide severe psychiatric disease associated with cognitive impairments. The aims of the present study are to investigate the preventive effects of alcoholic extract of sesame (Sesamum indicum L.) cake (SLE) and sesamol in a chronic unpredictable mild stress (CUMS)-induced mouse model. Oral administration of SLE (600 mg/kg/day) and sesamol (10 mg/kg/day) significantly restored CUMS-induced mice antidepressant-like behaviors, anhedonia, and anxiety. Importantly, supplementation of SLE and sesamol inhibited oxidative stress and improved serotonin levels in depressed mice brain. Moreover, SLE and sesamol treatment significantly prevented CUMS-induced memory loss in Y-maze and water-maze tests, which was consistent with enhanced the size of postsynaptic densities and postsynaptic density protein 95 (PSD-95) expression in mice hippocampus. These results illustrated that SLE and sesamol markedly improved CUMS-induced depression and memory loss, and provided novel insights into the mechanisms of sesamol and sesame crude extract on the regulation CUMS-induced depression and cognitive impairments.

Schisandrin rescues depressive-like behaviors induced by chronic unpredictable mild stress via GDNF/ERK1/2/ROS and PI3K/AKT/NOX signaling pathways in mice

The current study aimed to prove the antidepressant-like effects and the probable mechanisms of Schisandrin on depression, which induced by chronic unpredictable mild stress (CUMS) in mice. Four weeks of CUMS exposure resulted in depressive-like behavior, as indicated by the significant decrease in sucrose consumption and increase the immobility time in the forced swim test, but without any influence on the locomotor activity. Further, there were significant downregulations of GDNF/ERK1/2/ROS and PI3K/AKT/NOX signaling pathways in the hippocampus and prefrontal cortex in depressed mice. Treatment of mice with Schisandrin (30mg/kg) and Fluoxetine (10mg/kg) significantly ameliorated all the behavioral and biochemical changes induced by CUMS. These results suggest that Schisandrin produces an antidepressant-like effect in CUMS-induced mice, which possibly mediated, at least in part, by rectifying the signaling pathways of GDNF/ERK1/2/ROS and PI3K/AKT/NOX.

Antidepressant-like effects of sodium butyrate and its possible mechanisms of action in mice exposed to chronic unpredictable mild stress

Sodium butyrate (NaB) has exhibited neuroprotective activity. This study aimed to explore that NaB exerts beneficial effects on chronic unpredictable mild stress (CUMS)-induced depression-like behaviors and its possible mechanisms. The behavioral tests including sucrose preference test (SPT), open field test (OFT), tail suspension test (TST) and forced swimming test (FST) were to evaluate the antidepressant effects of NaB. Then changes of Nissl’s body in the hippocampus, brain serotonin (5-HT) concentration, brain-derived neurotrophic factor (BDNF) and tight junctions (TJs) proteins level were assessed to explore the antidepressant mechanisms. Our results showed that CUMS caused significant depression-like behaviors, neuropathological changes, and decreased brain 5-HT concentration, TJs protein levels and BDNF expression in the hippocampus. However, NaB treatment significantly ameliorated behavioral deficits of the CUMS-induced mice, increased 5-HT concentration, increased BDNF expression, and up-regulated Occludin and zonula occludens-1(ZO-1) protein levels in the hippocampus, which demonstrated that NaB could partially restore CUMS-induced blood–brain barrier (BBB) impairments. Besides, the pathologic changes were alleviated. In conclusion, these results demonstrated that NaB significantly improved depression-like behaviors in CUMS-induced mice and its antidepressant actions might be related with, at least in part, the increasing brain 5-HT concentration and BDNF expression and restoring BBB impairments.