ArticleCNS neuroscience & therapeutics2026
Elucidating Trigonelline's Therapeutic Mechanisms for Traumatic Brain Injury Through Integrated Network Pharmacology and In Vivo Validation.
Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Integrated WGCNA and Network Pharmacology Explore the Potential Mechanisms of D-Limonene in Alleviating Traumatic Brain Injury.International journal of molecular sciences · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundTraumatic brain injury (TBI) triggers complex pathological cascades, including inflammation, oxidative stress, apoptosis, and gliosis, particularly during the acute phase after injury. Trigonelline has been reported to exert neuroprotective effects in experimental models; however, its molecular mechanisms in acute TBI remain insufficiently defined.
objectiveThis study aimed to elucidate the molecular targets and mechanisms by which trigonelline attenuates acute TBI using an integrated network pharmacology and experimental validation approach.
methodsA trigonelline-target interaction network was constructed based on network pharmacology, followed by GO/KEGG analyses to predict the biological processes and pathways involved. Molecular docking was conducted to validate the binding affinity of trigonelline with key targets. Animal experiments were carried out to confirm the mechanistic predictions.
resultsNetwork pharmacology identified GAPDH, IL6, ALB, TNF, and IL1B as major hub genes associated with trigonelline. GO/KEGG analyses suggested that the neuroprotective effects of trigonelline against TBI primarily involved the MAPK and PI3K-Akt pathways. In vivo assays demonstrated that trigonelline treatment significantly reduced brain water content, inflammation, and oxidative stress levels within 72 h post-injury, while ameliorating histopathological damage, as confirmed by ELISA, HE, and LFB staining. TUNEL, NeuN, and FJB staining further revealed that trigonelline attenuated TBI-induced neuronal apoptosis. Western blotting demonstrated that trigonelline suppressed MMP-9 and AQP4 expression and attenuated the triggering of the MAPK signaling pathway.
conclusionBy attenuating MAPK signaling and apoptosis, trigonelline mitigates neural damage following TBI. The present findings provide experimental evidence supporting the neuroprotective effects of trigonelline in an acute TBI model.
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