ArticleCNS neuroscience & therapeutics2025
Network Pharmacology-Based and Experimental Validation Elucidate the Target Mechanism of Vinorine in Ameliorating Secondary Brain Injury After Intracerebral Hemorrhage.
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 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Computational pharmacovigilance of tranexamic acid: implications for intracerebral hemorrhage based on FAERS database and network toxicology.Frontiers in pharmacology · 2026Article
- Comments on "Network Pharmacology-Based and Experimental Validation Elucidate the Target Mechanism of Vinorine in Ameliorating Secondary Brain Injury After Intracerebral Hemorrhage".CNS neuroscience & therapeutics · 2025Article
- Network Pharmacology-Based and Experimental Validation Elucidate the Target Mechanism of Vinorine in Ameliorating Secondary Brain Injury After Intracerebral Hemorrhage.CNS neuroscience & therapeutics · 2025Article
- The role of MMPs in intracerebral hemorrhage.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
backgroundIntracerebral hemorrhage (ICH) is a severe stroke subtype associated with high mortality and long-term disability, for which no effective treatment currently exists. Vinorine (Vin), a monoterpene indole alkaloid derived from Rauvolfia reflexa, has been traditionally used for age-related neurological disorders, yet its therapeutic potential and mechanisms in ICH remain unclear.
methodsAn ICH mouse model was established via intracranial collagenase injection. Vin was administered intraperitoneally at varying doses, and its effects on motor function, sensory deficits, and neural regeneration were evaluated. Network pharmacology was employed to predict potential targets and pathways, followed by validation through molecular docking, in vivo experiments, and in vitro assays.
resultsNetwork pharmacology identified four core targets and 35 related pathways, with JAK2 as a central node. In vivo, Vin significantly improved motor deficits, reduced cerebral edema, preserved blood-brain barrier integrity, and promoted hematoma resolution. These effects were mediated through modulation of the CXCR2-JAK-STAT axis and suppression of JAK2 phosphorylation. In vitro, Vin inhibited JAK-STAT activation in microglia, downregulated MMP expression, and facilitated the transition from M1 to M2 phenotypic polarization. Additionally, Vin enhanced the expression of neuronal markers (NF200, PSD95, GAP43) and reduced neuronal apoptosis.
conclusionVin attenuates neurological deficits after ICH likely by inhibiting MMP expression in microglia via regulation of the CXCR2-JAK-STAT pathway. These findings highlight the therapeutic potential of Vin and provide mechanistic support for its further development as a treatment for ICH.
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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.