ArticleMetabolic brain disease2025
Integrating network pharmacology and experimental validation deciphers the improving effect and mechanisms of Shenwu Yizhi capsule on cognitive impairment in vascular dementia rats.
Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Emodin Suppresses the RAGE/ROCK1 Pathway to Modulate the Oligodendrocyte Lineage and Ameliorate Demyelination in Vascular Dementia Rats.CNS neuroscience & therapeutics · 2026Article
- Citronellal Alleviates Cognitive Impairment by Inhibiting NHE1-Mediated Mitochondrial Damage in Vascular Dementia.Applied biochemistry and biotechnology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
The therapeutic mechanisms of Shenwu Yizhi Capsule (SWYZC), a widely used treatment for vascular dementia (VD), remain unclear. This study integrated network pharmacology and experimental methods to elucidate the effects and mechanisms of SWYZC on cognitive function in VD rats. A VD model was established via bilateral common carotid artery occlusion (2-VO). Cognitive function was evaluated using the Morris water maze (MWM), and hippocampal neuronal morphology was assessed via hematoxylin-eosin (HE) staining. Active compounds and targets of SWYZC were identified using the TCMSP, PubChem, and Swiss Target Prediction databases, while VD-related targets were retrieved from OMIM, TTD, and GeneCards. Venny 2.1.0 identified overlapping targets between SWYZC and VD. The STRING database analyzed protein-protein interaction (PPI) networks, and the DAVID database conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Apoptosis and dendritic function were evaluated to explore therapeutic mechanisms. Molecular docking was performed using AutoDock Vina. SWYZC significantly ameliorated cognitive deficits and hippocampal neuronal damage. PPI network analysis identified 20 key targets between SWYZC and VD, including TP53, SRC, CASP3, etc. GO and KEGG analyses indicated that apoptosis, inflammation, and synaptic injury targets were central to SWYZC's therapeutic effects on VD. Moreover, experimental validation demonstrated that SWYZC significantly upregulated PSD95 and PGC-1α expression while downregulated Cleaved Caspase-3, Bax, and connexin43 (CX43) levels. Molecular docking indicated that celabenzine exhibited strong binding to Bax and CX43. Collectively, SWYZC improves memory function and mitigates hippocampal neuronal damage in VD rats by inhibiting apoptosis and promoting synapse formation.
Indexed as
Identifiers
40913651What Socratic holds
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.