Purification engineering technology research center of Sichuan Province Natural Medicine
四川省天然药物分离纯化工程技术研究中心
文献
Hanxiao Wang, et al."Modulation of Pseudomonas aeruginosa-induced avoidance behavior by Shen Qi pills via mitogen-activated protein kinase PMK-1 and forkhead box protein O DAF-16 in Caenorhabditis elegans."Phytomedicine 140.(2025):156585-156585.
本文来自: 发布时间:2025-12-22
发表期刊: Phytomedicine
发表时间:2025
Abstract:
Background
Avoidance behavior is one of the core features of anxiety and related in-depth study can help to reveal the biological basis of these disorders. In recent years, traditional Chinese medicine has incorporated Shen Qi pills to treat neuropsychiatric disorders, such as depression and post-traumatic stress, and has achieved significant therapeutic effects. However, its specific mechanism of action is still unclear.
Purpose
The aim of this study was to link the avoidance phenotype to psychiatric disorders by utilizing the Caenorhabditis elegans as a biological model, revealing the potential common mechanisms underlying the treatment of these disorders with Shen Qi pills.
Methods
Avoidance behavior and immunity of C. elegans as a phenotypic entry point to explore the molecular mechanisms by which Shen Qi pills affects avoidance behavior with the help of pmk-1 and daf-16 mutants and RNA interference techniques.
Results
We found that the intervention of Shen Qi pills can delay the avoidance behavior of C. elegans to P. aeruginosa, improve the immunity level, and reduce the up-regulation of pmk-1 and daf-16 genes induced by P. aeruginosa. Shen Qi pills did not improve the immunity of pmk-1 mutant but could still enhance the immunity of daf-16 mutant. After daf-16 knockout, Shen Qi pills could not delay its avoidance behavior, which was consistent with the results shown in the neuron-specific silencing of daf-16 C. elegans.
Conclusion
These findings reveal the conclusion that Shen Qi pills regulate the avoidance behavior of C. elegans induced by P. aeruginosa via PMK-1 and DAF-16, with the latter acting directly on neurons independent of immune pathways.
https://doi.org/10.1016/j.phymed.2025.156585
