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Electroacupuncture ameliorates post-traumatic stress disorder in rats via a mechanism involving the BDNF-TrkB signaling pathway

机译:通过涉及BDNF-TRKB信号传导途径的机制,电针改善了大鼠的创伤后应激障碍

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Post-traumatic stress disorder (PTSD) is a mental health condition triggered by a terrifying event, causing flashbacks, nightmares and severe anxiety. It develops in individuals who have experienced a shocking, scary, or dangerous event. Electroacupuncture is reported to be effective for the treatment of PTSD. The present study was carried out to investigate the protective effect of electroacupuncture in a rat model of PTSD, and the mechanism involved. Specific-pathogen free male Sprague Dawley rats (n = 30) weighing 180-220 g (mean weight = 200 +/- 20 g) were randomly assigned to three groups of ten rats each: control group, single-prolonged stress (SPS) group, and treatment group. The treatment group rats received electroacupuncture. Changes in PTSD-like behavior were assessed using locomotor activity, elevated plus-maze (EPM) and fear conditioning tests. The mRNA and protein expressions of brain-derived neurotrophic factor (BDNE) and tropomyosin receptor kinase B (TrkB) were determined using real-time quantitative polymerise chain reaction (qRT-PCR) and Western blotting, respectively. Co-immunoprecipitation (Co-IP) was used to measure BDNIF and TrkB binding interaction, while chromatin immunoprecipitation (CLAP) was used to evaluate the binding between cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) and its target genes. Electroacupuncture significantly creased locomotor activity and exploratory behavior, but significantly reduced general fear and anxiety in SYS rats (p < 0.05). It also significantly upregulated the mRNA and protein expressions of BDNI, and TrkB, and increased the binding of BDNI, to its receptor TrkB <0.05). Electroacupuncture significantly increased the binding of CREB to BDNT promoter region (p < 0.05). Electroacupuncture ameliorates PTSD in rats via a mechanism involving the BDNE-TrkB signaling pathway.
机译:创伤后应激障碍(PTSD)是一种由恐怖事件引发的心理健康状况,可导致倒叙、噩梦和严重焦虑。它发生在经历过令人震惊、恐怖或危险事件的个人身上。据报道,电针治疗PTSD是有效的。本研究旨在探讨电针对创伤后应激障碍大鼠模型的保护作用及其机制。将体重180-220克(平均体重200+/-20克)的无特定病原体雄性Sprague-Dawley大鼠(n=30)随机分为三组,每组10只:对照组、单一长期应激(SPS)组和治疗组。治疗组大鼠接受电针治疗。通过运动活动、高架+迷宫(EPM)和恐惧条件反射测试评估PTSD样行为的变化。采用实时定量聚合酶链反应(qRT PCR)和免疫印迹法分别检测脑源性神经营养因子(BDNE)和原肌球蛋白受体激酶B(TrkB)的mRNA和蛋白质表达。共免疫沉淀(Co-IP)用于检测BDNIF和TrkB的结合相互作用,而染色质免疫沉淀(CLAP)用于评价环磷酸腺苷(cAMP)反应元件结合蛋白(CREB)与其靶基因之间的结合。电针显著增加了SYS大鼠的运动活动和探索行为,但显著降低了一般恐惧和焦虑(p<0.05)。它还显著上调了BDNI和TrkB的mRNA和蛋白质表达,并增加了BDNI与其受体TrkB的结合(TrkB<0.05)。电针显著增加CREB与BDNT启动子区的结合(p<0.05)。电针通过涉及BDNE-TrkB信号通路的机制改善大鼠PTSD。

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