ArticleCNS neuroscience & therapeutics2025
Elucidating the Mechanism of Emodin in Treating Post-Stroke Depression Through Network Pharmacology and Animal Experiments.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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Who cites it
1 citing paper in PubMed.
- Elucidating the Mechanism of Emodin in Treating Post-Stroke Depression Through Network Pharmacology and Animal Experiments.CNS neuroscience & therapeutics · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
objectiveEvaluate the mechanism of Emodin therapy for Post-stroke depression (PSD) using network pharmacology and animal experiments.
methodsFirstly, the effectiveness of Em in treating PSD was confirmed by constructing a PSD rat model. Then, network pharmacology and molecular docking techniques were used to analyze the potential signaling pathways and targets of Em therapy for PSD. Further exploration and validation were conducted using the PSD rat model. Finally, the expressions of tissue plasminogen activator (tPA), matrix metallopeptidase-9 (MMP9), furin, and proprotein convertases (PC) in the hippocampus and medial prefrontal cortex (mPFC) were further detected.
resultsEm exhibited significant neuroprotective and antidepressant effects on PSD. Network pharmacology analysis revealed that Em may exert pharmacological effects on PSD through 47 core targets. These targets were involved in multiple signaling pathways. Molecular docking studies demonstrated that Em had a strong binding affinity for core targets. Animal experiments further indicated that Em could regulate the expression of precursor brain-derived neurotrophic factor (proBDNF) and mature BDNF (mBDNF) in the hippocampus and mPFC, ameliorating apoptosis. In addition, Em could upregulate the expression of tPA gene and protein in the hippocampus and mPFC, as well as upregulate the expression of Furin gene and protein in the mPFC. This confirmed that the balance regulation of proBDNF/mBDNF depends on tPA and Furin.
conclusionThe therapeutic effects of Em on PSD are multi-targets and multi-pathways. Em may exert therapeutic effects on PSD by binding to the core target, BDNF. The mechanism may be to regulate the balance proBDNF/mBDNF via tPA and Furin, improving apoptosis.
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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 Socratic graph.