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首页> 美国卫生研究院文献>Experimental and Therapeutic Medicine >Estrogen administration attenuates post-stroke depression by enhancing CREB/BDNF/TrkB signaling in the rat hippocampus
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Estrogen administration attenuates post-stroke depression by enhancing CREB/BDNF/TrkB signaling in the rat hippocampus

机译：雌激素给药通过增强大鼠海马中的CREB ​​/ BDNF / TRKB信号传导来衰减卒中后抑郁症

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A previous study demonstrated that 17β-estradiol (E2), which is an antidepressant, can ameliorate post-stroke depression (PSD); however, the underlying mechanisms governing this remain largely unknown. Therefore, the present study developed a PSD model in rats, which was induced by left middle cerebral artery occlusion followed by exposure to chronic mild stress for 2 weeks. The results revealed that the activity of the cAMP response element-binding protein (CREB), a cellular transcription factor, and the associated brain-derived neurotrophic factor (BDNF)/tyrosine kinase B (TrkB) signaling were all attenuated in the hippocampus in PSD rats. The depression-like behaviors were significantly improved after treatment with E2, along with increased CREB and the BDNF/TrkB signaling activity. These results provide novel insight into the molecular basis of PSD, and suggest the potential involvement of CREB/BDNF/TrkB signaling in E2-mediated improvement of PSD in rats.
机译：先前的研究表明，17β-雌二醇（E2）是抗抑郁药，可以改善行程后抑郁（PSD）;但是，管理这一目标的基本机制仍然很大程度上是未知的。因此，本研究在大鼠中开发了一种PSD模型，其被左中脑动脉闭塞诱导，然后暴露于慢性轻度胁迫2周。结果表明，阵营响应元件结合蛋白（CREB），细胞转录因子和相关的脑衍生的神经营养因子（BDNF）/酪氨酸激酶B（TRKB）信号传导的活性全部衰减在PSD中的海马中老鼠。用E2处理后，抑郁症样行为随着CREB的增加和BDNF / TRKB信号传导活性而显着改善。这些结果提供了对PSD的分子基础的新颖洞察力，并提示CREB ​​/ BDNF / TRKB信号传导在大鼠e2介导的PSD改善中的潜在累及。

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