<i>Eleutheroside E</i> Enhances the Long-Term Memory of Radiation-Damaged <i>C. elegans</i> through G-Protein-Coupled Receptor and Neuropeptide Signaling Pathways

Abstract

<i>Eleutheroside E</i> (<i>EE</i>), a principal active compound of <i>Acanthopanax senticosus</i>, has been shown to have a certain neuromodulation effect. Our previous study indicates that <i>EE</i> 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 <i>C. elegans</i> model to illuminate the property and mechanism of <i>EE</i> protecting against nerve damage caused by radiation. Here, we found that <i>EE</i> significantly improved the long-term memory of radiation-damaged <i>C. elegans</i>. Through transcriptome sequencing, the results showed that <i>EE</i> protected radiation-damaged <i>C. elegans</i> mainly through G-protein-coupled receptor and neuropeptide signaling pathways. Further research indicated that <i>EE</i> 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 <i>C. elegans</i>. In addition, the activity of G_qα and neuropeptides in AWC neurons and the activity of CREB in AIM neurons might be crucial for <i>EE</i> to function.