Research Paper Volume 15, Issue 16 pp 8433—8443
Catapol reduced the cognitive and mood dysfunctions in post-stroke depression mice via promoting PI3K-mediated adult neurogenesis
- 1 Department of Neurosurgery, General Hospital of Taiyuan Iron and Steel Co, Taiyuan, China
- 2 Medical Laboratory, Shanxi Province Pediatric Hospital, Taiyuan, China
- 3 Department of Endocrinology, General Hospital of Taiyuan Iron and Steel Co, Taiyuan, China
- 4 Department of Anesthesiology, Shanxi Bethune Hospital, Taiyuan, China
Received: February 3, 2023 Accepted: May 9, 2023 Published: August 29, 2023
https://doi.org/10.18632/aging.204979How to Cite
Copyright: © 2023 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Adult hippocampal neurogenesis provides a regenerative resource for neural tissue and enhances neural plasticity, which is beneficial for brain functional rehabilitation post stroke. Recently, an increasing number of metabolic drugs have been reported to attenuate behavioral symptoms in neurodegeneration or psychiatric disorders via promoting adult hippocampal neurogenesis. Bioeffects of catapol show its potential as an antidiabetic though it has been previously widely indicated to perform the neuroprotective functions. However, the systematic evidence to support the behavioral effects of catapol to PSD model and what is the role of adult neurogenesis in such effects remains unexplored. In current study, we created the PSD model by combining MCAO procedure and CORT feeding. The treatment of catapol strikingly reduced the depressive/anxiety behavior in PSD model. Moreover, treatment of catapol also improved the cognitive functions. Immunofluorescence indicates that catapol could promote adult hippocampal neurogenesis in PSD model, and TMZ treatment further confirmed the role of the hippocampal neurogenesis in catapol’s therapeutic effects to PSD. Cultural neurons also indicates that PI3K is the key signal in regulating catapol mediated neurogenesis. By administrating the PI3K specific inhibitor, we found that PI3K is the key to mediate the behavioral effects of catapol to PSD. In conclusion, catapol could perform as the effective drug to treat PSD via the PI3K mediated adult hippocampal neurogenesis.