β-asarone relieves chronic unpredictable mild stress induced depression by regulating the extracellular signal-regulated kinase signaling pathway.

Abstract

The present study aimed to investigate the effect of β-asarone treatment in a rat model of depression induced by chronic unpredictable mild stress (CUMS) and to further explore the underlying molecular mechanisms. A rat model of depression was established by subjecting rat to CUMS and treated with various concentrations of β-asarone (12.5, 25 and 50 mg/kg/day) and fluoxetine (20 mg/kg/day). Next, behavioral tests, including an open field, sucrose preference and forced swimming tests, were performed. In addition, the apoptosis of hippocampal neuronal cells was determined by flow cytometry, gene expression levels were detected by reverse transcription-quantitative polymerase chain reaction and protein levels were determined by western blot assay. The results revealed that β-asarone significantly mitigated CUMS-induced depression-like behavior, evidenced by the increased sucrose intake, crossing and rearing numbers, and decreased immobility time in the forced swimming test. Furthermore, β-asarone significantly decreased the apoptosis rate of hippocampal neuronal cells in rats subjected to CUMS. β-asarone was also found to enhance CREB, BDNF, Trk-B and Bcl-2 levels, and reduce Bad level in the hippocampus of CUMS-treated rats. In addition, the activation of extracellular signal-regulated kinase pathway inhibited by CUMS was promoted by β-asarone treatment. In conclusion, the present study findings indicated the antidepressant-like effects of β-asarone on CUMS-induced depression in rats.