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Icariin sustains the proliferation and differentiation of Aβ25-35-treated hippocampal neural stem cells via the BDNF-TrkB-ERK/Akt signaling pathway.
Neurological Research ( IF 1.9 ) Pub Date : 2020-07-30 , DOI: 10.1080/01616412.2020.1792701
Quan Lu 1 , Hailing Zhu 2 , Xuejiao Liu 3 , Congfeng Tang 1
Affiliation  

ABSTRACT

Objectives

Icariin (ICA) can be potentially used to treat Alzheimer’s disease (AD), but the mechanism was not clear. The current study explored the effects of ICA on hippocampal neural stem cells, aiming to provide a comprehensive basis for its clinical application.

Methods

Hippocampal neural stem cells were isolated from newborn rats and their differentiation ability was evaluated by performing immunofluorescence staining. Next, Aβ cell model was constructed by treating the cells with Aβ25-35, and then the model was further treated by ICA or shBDNF or the two in combination. The viability and differentiation of the cells were, respectively, analyzed by 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-Diphenyltetrazolium Bromide (MTT) and flow cytometry. The expression of BDNF-TrkB-ERK/Akt signaling pathway was assessed by quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot (WB).

Results

The hippocampal neural stem cells can differentiate into neurons and astrocytes. ICA effectively promoted the viability and differentiation of Aβ cell models. The expression levels of BDNF and TrkB in Aβ cell models were obviously decreased, which were noticeably increased by ICA. Moreover, BDNF knockdown further inhibited the viability and differentiation of Aβ model cells, which could be reversed by ICA. BDNF knockdown not only suppressed the expressions of BDNF and TrkB in Aβ cell models but also effectively prevented the phosphorylation of ERK/Akt; however, these phenomena were significantly alleviated by ICA treatment.

Discussion

ICA promoted the proliferation and differentiation of Aβ25-35-treated hippocampal neural stem cells through BDNF-TrkB-ERK/Akt signaling pathway. The current findings might contribute to the treatment of AD.



中文翻译:

淫羊藿苷通过 BDNF-TrkB-ERK/Akt 信号通路维持 Aβ25-35 处理的海马神经干细胞的增殖和分化。

摘要

目标

淫羊藿苷 (ICA) 可潜在用于治疗阿尔茨海默病 (AD),但其机制尚不清楚。本研究探讨ICA对海马神经干细胞的影响,旨在为其临床应用提供综合依据。

方法

从新生大鼠中分离海马神经干细胞,通过免疫荧光染色评价其分化能力。接下来,用Aβ 25-35处理细胞构建Aβ细胞模型,然后进一步用ICA或shBDNF或两者联合处理模型。分别通过 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-Diphenyltetrazolium Bromide (MTT) 和流式细胞术分析细胞的活力和分化。通过定量实时聚合酶链反应 (qRT-PCR) 或蛋白质印迹 (WB) 评估 BDNF-TrkB-ERK/Akt 信号通路的表达。

结果

海马神经干细胞可分化为神经元和星形胶质细胞。ICA有效地促进了Aβ细胞模型的活力和分化。Aβ细胞模型中BDNF和TrkB的表达水平明显降低,ICA显着升高。此外,BDNF 敲低进一步抑制了 Aβ 模型细胞的活力和分化,这可以被 ICA 逆转。BDNF敲低不仅抑制了Aβ细胞模型中BDNF和TrkB的表达,而且有效阻止了ERK/Akt的磷酸化;然而,ICA 治疗显着缓解了这些现象。

讨论

ICA通过BDNF-TrkB-ERK/Akt信号通路促进Aβ25-35处理的海马神经干细胞的增殖和分化。目前的研究结果可能有助于 AD 的治疗。

更新日期:2020-07-30
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