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

机译:β-细辛醚通过调节细胞外信号调节激酶信号通路减轻慢性应激反应所致的抑郁

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摘要

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.
机译:本研究旨在研究β-细辛醚治疗在慢性不可预测的轻度应激(CUMS)诱发的抑郁症大鼠模型中的作用,并进一步探讨其潜在的分子机制。通过使大鼠接受CUMS建立抑郁症的大鼠模型,并用各种浓度的β-细辛醚(12.5、25和50 mg / kg / day)和氟西汀(20 mg / kg / day)处理。接下来,进行了行为测试,包括开放视野,蔗糖偏爱和强迫游泳测试。此外,通过流式细胞术测定海马神经元细胞的凋亡,通过逆转录-定量聚合酶链反应检测基因表达水平,并通过蛋白质印迹法测定蛋白质水平。结果表明,在强迫游泳试验中,蔗糖摄入量,交叉和饲养次数的增加以及不动时间的减少证明了β-花生四烯酸可显着缓解CUMS诱导的抑郁样行为。此外,β-asaron显着降低了CUMS大鼠的海马神经元凋亡率。还发现β-细辛醚可提高CUMS治疗的大鼠海马中的CREB,BDNF,Trk-B和Bcl-2水平,并降低Bad水平。此外,β-细辛醚处理可促进CUMS抑制细胞外信号调节激酶途径的激活。总之,本研究结果表明,β-细辛醚对大鼠CUMS诱发的抑郁症具有抗抑郁样作用。

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