Electroacupuncture Pretreatment Ameliorates PTSD-Like Behaviors in Rats by Enhancing Hippocampal Neurogenesis via the Keap1/Nrf2 Antioxidant Signaling Pathway

Electroacupuncture Pretreatment Ameliorates PTSD-Like Behaviors in Rats by Enhancing Hippocampal Neurogenesis via the Keap1/Nrf2 Antioxidant Signaling Pathway
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电针预处理通过 Keap1/Nrf2 抗氧化信号通路增强海马神经发生改善大鼠 PTSD 样行为

DOI:
10.3389/fncel.2019.00275
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发表时间:
2019-06
影响因子:
5.3
通讯作者:
Peng Zheng wu
Peng Zheng wu
中科院分区:
医学2区
文献类型:
--
作者:
Zhou Cui hong;Xue Fen;Xue Shan shan;Sang Han fei;Liu Ling;Wang Ying;Cai Min;Zhang Zhang Jin;Tan Qing rong;Wang Hua ning;Peng Zheng wu

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电针(EA)预处理是对多种脑部疾病具有临床应用价值的一种疗法。然而,它是否以及通过何种确切的分子机制改善创伤后应激障碍(PTSD)仍不清楚。在本研究中,大鼠……(最后一个单词“rec”不完整,无法准确翻译其所在的完整句子)
Electroacupuncture (EA) pretreatment is a clinically useful therapy for several brain disorders. However, whether and via which exact molecular mechanisms it ameliorates post-traumatic stress disorder (PTSD) remains unclear. In the present study, rats received EA stimulation for seven consecutive days before exposure to enhanced single prolonged stress (ESPS). Anxiety-like and fear learning behaviors; hippocampal neurogenesis; the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), Kelch-like ECH-associated protein 1 (keap1), and heme oxygenase 1 (HO-1); and the activity of AMP-activated kinase (AMPK) were evaluated at 14 days after ESPS. EA pretreatment improved hippocampal neurogenesis and ameliorated anxiety-like behaviors in ESPS-treated rats. EA pretreatment also increased the expression of Nrf2 and HO-1 and the activity of AMPK. Furthermore, Nrf2 knockdown by a short hairpin RNA affected anxiety-like behaviors and expression of neuroprotective markers (BDNF, DCX) in a manner similar to ESPS alone and dampened the neuroprotective effects of EA pretreatment. In contrast, Keap1 knockdown increased the expression of HO-1, improved hippocampal neurogenesis, and alleviated PTSD-like behaviors. Altogether, our results suggest that EA pretreatment ameliorates ESPS-induced anxiety-like behaviors and prevents hippocampal neurogenesis disruption in a rat model of PTSD possibly through regulation of the keap1/Nrf2 antioxidant defense pathway.
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