ArticleInternational journal of molecular sciences2023
Exploration of the Core Pathways and Potential Targets of Luteolin Treatment on Late-Onset Depression Based on Cerebrospinal Fluid Proteomics.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Optimization of potential targets for antidepressant Chinese medicines: AI and multi-omics methods.Chinese medicine · 2026Review
- Cerebrospinal Fluid Proteome Reveals Dysregulation of Lysosomal and Axonal Proteins in Neurosyphilis.Journal of proteome research · 2026Article
- Protective Effect of luteolin on CLP-induced Sepsis-associated Encephalopathy via Inhibiting p38 MAPK Signalling in a Rat Model.Molecular neurobiology · 2026Article
- Association between sleep and meteorology in late-onset depression patients.BMC psychiatry · 2025Article
- Luteolin and its antidepressant properties: From mechanism of action to potential therapeutic application.Journal of pharmaceutical analysis · 2025Review
- Luteolin ameliorates chronic stress-induced depressive-like behaviors in mice by promoting the Arginase-1Acta pharmacologica Sinica · 2025Article
- Review
- Luteolin alleviates depression-like behavior by modulating glycerophospholipid metabolism in the hippocampus and prefrontal cortex of LOD rats.CNS neuroscience & therapeutics · 2024Article
- The therapeutic potential of traditional Chinese medicine in depression: focused on the modulation of neuroplasticity.Frontiers in pharmacology · 2024Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Cognitive deficiency is one of the fundamental characteristics of late-onset depression (LOD). Luteolin (LUT) possesses antidepressant, anti-aging, and neuroprotective properties, which can dramatically enhance cognition. The altered composition of cerebrospinal fluid (CSF), which is involved in neuronal plasticity and neurogenesis, directly reflects the physio-pathological status of the central nervous system. It is not well known whether the effect of LUT on LOD is in association with a changed CSF composition. Therefore, this study first established a rat model of LOD and then tested the therapeutic effects of LUT using several behavioral approaches. A gene set enrichment analysis (GSEA) was used to evaluate the CSF proteomics data for KEGG pathway enrichment and Gene Ontology annotation. We combined network pharmacology and differentially expressed proteins to screen for key GSEA-KEGG pathways as well as potential targets for LUT therapy for LOD. Molecular docking was adopted to verify the affinity and binding activity of LUT to these potential targets. The outcomes demonstrated that LUT improved the cognitive and depression-like behaviors in LOD rats. LUT may exert therapeutic effects on LOD through the axon guidance pathway. Five axon guidance molecules-
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