ArticleAging2023
Catapol reduced the cognitive and mood dysfunctions in post-stroke depression mice via promoting PI3K-mediated adult neurogenesis.
Article in Aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Decreased hippocampal neurogenesis and post-stroke depression.Frontiers in psychiatry · 2026Review
- Article
- Elucidating the Mechanism of Emodin in Treating Post-Stroke Depression Through Network Pharmacology and Animal Experiments.CNS neuroscience & therapeutics · 2025Article
- Multifaceted therapeutic potentials of catalpol, an iridoid glycoside: an updated comprehensive review.Inflammopharmacology · 2025Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.