Objective

The hippocampus is thought to be a vulnerable target of microwave exposure. The aim of the present study was to investigate whether 20-hydroxyecdysone (20E) acted as a fate regulator of adult rat hippocampal neural stem cells (NSCs). Furthermore, we investigated if 20E attenuated high power microwave (HMP) radiation-induced learning and memory deficits.

Methods

Sixty male Sprague-Dawley rats were randomly divided into three groups: normal controls, radiation treated, and radiation+20E treated. Rats in the radiation and radiation+20E treatment groups were exposed to HPM radiation from a microwave emission system. The learning and memory abilities of the rats were assessed using the Morris water maze test. Primary adult rat hippocampal NSCs were isolated in vitro and cultured to evaluate their proliferation and differentiation. In addition, hematoxylin & eosin staining, western blotting, and immunofluorescence were used to detect changes in the rat brain and the proliferation and differentiation of the adult rat hippocampal NSCs after HPM radiation exposure.

Results

The results showed that 20E induced neuronal differentiation of adult hippocampal NSCs from HPM radiation-exposed rats via the Wnt3a/β-catenin signaling pathway in vitro. Furthermore, 20E facilitated neurogenesis in the subgranular zone of the rat brain following HPM radiation exposure. Administration of 20E attenuated learning and memory deficits in HPM radiation-exposed rats and frizzled-related protein (FRZB) reduced the 20E-induced nuclear translocation of β-catenin, while FRZB treatment also reversed 20E-induced neuronal differentiation of NSCs in vitro.

Conclusion

These results suggested that 20E was a fate regulator of adult rat hippocampal NSCs, where it played a role in attenuating HPM radiation-induced learning and memory deficits.

中文翻译：

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20-羟基蜕皮激素改善高功率微波辐射暴露大鼠成年海马神经干细胞的神经元分化

客观的

海马体被认为是微波暴露的脆弱目标。本研究的目的是调查 20-羟基蜕皮激素 (20E) 是否作为成年大鼠海马神经干细胞 (NSC) 的命运调节剂。此外，我们调查了 20E 是否能减弱高功率微波 (HMP) 辐射引起的学习和记忆缺陷。

方法

将60只雄性Sprague-Dawley大鼠随机分为三组：正常对照组、放射治疗组和放射+20E治疗组。将辐射和辐射+20E 处理组中的大鼠暴露于来自微波发射系统的 HPM 辐射。使用Morris水迷宫测试评估大鼠的学习和记忆能力。体外分离原代成年大鼠海马神经干细胞并培养以评估其增殖和分化。此外，采用苏木精-伊红染色、western blotting和免疫荧光检测HPM辐射暴露后大鼠大脑的变化以及成年大鼠海马NSCs的增殖和分化情况。

结果

结果表明，20E在体外通过Wnt3a/β-catenin信号通路诱导HPM辐射暴露大鼠成年海马NSCs的神经元分化。此外，在 HPM 辐射暴露后，20E 促进了大鼠大脑颗粒下区的神经发生。给予 20E 可减轻 HPM 辐射暴露大鼠的学习和记忆缺陷，并且卷曲相关蛋白 (FRZB) 可减少 20E 诱导的 β-连环蛋白核转位，而 FRZB 治疗也可逆转 20E 诱导的 NSC体外神经元分化。

结论

这些结果表明，20E 是成年大鼠海马神经干细胞的命运调节剂，在减轻 HPM 辐射引起的学习和记忆缺陷方面发挥了作用。