Estrogen administration attenuates post‑stroke depression by enhancing CREB/BDNF/TrkB signaling in the rat hippocampus
- Huigang Jiang
- Li Xiao
- Kunlin Jin
- Bei Shao
Affiliations: Department of Neurology, Yiwu City Center Hospital, Wenzhou Medical University, Yiwu, Zhejiang 322000, P.R. China, Department of Neurology, Shaoyang City Center Hospital, Shaoyang, Hunan 422000, P.R. China, Department of Neurology, First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China
- Published online on: February 26, 2021 https://doi.org/10.3892/etm.2021.9850
Copyright: © Jiang
et al. This is an open access article distributed under the
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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.