Abstract
ObjectiveResveratrol(RES) is a natural polyphenol which possesses an anti-depressant effect. However, the mechanisms of its anti-depressant effect remain unclear. The aim of the study is to investigate the potential mechanisms in the neuro-protective efficiency in the corticosterone-induced pheochromacytoma 12 (PC12) cells.MethodsPC12 cells were treated with 200 μM of corticosterone in the absence or presence of different concentrations of RES for 24 h. Then, cell viability was measured by Cell Counting Kit-8 assay. Apoptosis of PC12 cells was measured by Annexin V-FITC and Propidium iodide (PI) labelling. The expression of apoptosis-related proteins including Bax, Bcl-2, caspase-3 was determined by western blotting.ResultsThe results showed that treatment with 200 μM of corticosterone induced cytotoxicity in PC12 cells. However, different concentrations of RES (2.5μmol/L, 5μmol/L and 10 μmol/L) significantly increased the cell viability, suppressed the apoptosis of PC12 cells, down-regulated Bax and caspase-3 protein expression, and up-regulated Bcl-2 protein expression, compared to the model group (p<0.05).ConclusionResveratrol has a protective effect on corticosterone-induced neurotoxicity in PC12 cells, which may be related to the apoptosis via inhibition of apoptosis-related proteins and displays the antidepressant-like effect.
Highlights
Depression is one of the most common mental disorders, more than 300 million people worldwide suffering from depression
pheochromacytoma 12 (PC12) cells were treated with 200 μM of corticosterone in the absence or presence of different concentrations of RES for 24 h
Resveratrol has a protective effect on corticosteroneinduced neurotoxicity in PC12 cells, which may be related to the apoptosis via inhibition of apoptosis-related proteins and displays the antidepressant-like effect
Summary
Depression is one of the most common mental disorders, more than 300 million people worldwide suffering from depression. Depression leads to a decline in social ability and causes severe burden [1,2]. Some acceptable mechanisms include the monoamine neurotransmitter hypothesis, the hypothalamic-pituitaryadrenal (HPA) axis activation hypothesis, nerve-inflammation hypothesis, cytokine hypothesis [3,4,5]. Antidepressant drugs such as serotonin reuptake inhibitors can inhibit the activation of HPA axis [6,7]. Long-term use antidepressant can cause lots of side effects. Researches have been shown that RES could improve depression behavior [12,13,14,15,16]. The mechanisms may associate with the regulation of brain derived neurotrophic fatcor, HPA axis, an increase of 5-HT, reduction of inflammatory factors, neurons protection [17,18,19,20].the exact mechanism is still unknown
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