Eleutheroside E (EE), a principal active compound of Acanthopanax senticosus, has been shown to have a certain neuromodulation effect. Our previous study indicates that EE protects nerve damage caused by radiation. However, its specific function and underlying mechanism remain unknown. Therefore, the objective of this study is to apply the C. elegans model to illuminate the property and mechanism of EE protecting against nerve damage caused by radiation. Here, we found that EE significantly improved the long-term memory of radiation-damaged C. elegans. Through transcriptome sequencing, the results showed that EE protected radiation-damaged C. elegans mainly through G-protein-coupled receptor and neuropeptide signaling pathways. Further research indicated that EE affected the activity of CREB by cAMP-PKA, G_qα-PLC, and neuropeptide signaling pathways to ultimately improve the long-term memory of radiation-damaged C. elegans. In addition, the activity of G_qα and neuropeptides in AWC neurons and the activity of CREB in AIM neurons might be crucial for EE to function.

中文翻译：

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Eleutheroside E 通过 G 蛋白偶联受体和神经肽信号通路增强受辐射损伤的秀丽隐杆线虫的长期记忆

Eleutheroside E ( EE ) 是刺五加的主要活性化合物，已被证明具有一定的神经调节作用。我们之前的研究表明，EE可以保护辐射引起的神经损伤。然而，其具体功能和潜在机制仍然未知。因此，本研究的目的是应用秀丽隐杆线虫模型来阐明EE防止辐射引起的神经损伤的特性和机制。在这里，我们发现EE显着改善了受辐射损伤的秀丽隐杆线虫的长期记忆。通过转录组测序，结果表明EE主要通过 G 蛋白偶联受体和神经肽信号通路保护受辐射损伤的秀丽隐杆线虫。进一步的研究表明，EE通过 cAMP-PKA、G _q α-PLC 和神经肽信号通路影响 CREB ​​的活性，最终改善受辐射损伤的秀丽隐杆线虫的长期记忆。此外，AWC 神经元中 G _q α 和神经肽的活性以及 AIM 神经元中 CREB ​​的活性可能对EE的功能至关重要。