ArticleMolecular neurobiology2025
Vinpocetine Ameliorates Neuronal Injury After Cold-Induced Traumatic Brain Injury in Mice.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Vinpocetine-An "Old" Drug with a New Face: Moving Toward a Better Understanding of Its Neuroprotective Mechanism of Action.Biomolecules · 2026Review
- Immediate impacts of low-temperature exposure on cardiac autonomic modulation, neuromuscular efficiency, and postural stability in older adults Yangko dancers - a randomized controlled trial.Frontiers in physiology · 2026Article
- A bioengineered vinpocetine- and menstrual blood stem cell-loaded neural conduit for treating peripheral nerve injury after bone fractures.Journal of materials science. Materials in medicine · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
Traumatic brain injury (TBI), also known as intracranial injury, is a common condition with the highest incidence rate among neurodegenerative disorders and poses a significant public health burden. Various methods are used in the treatment of TBI, but the effects of cold-induced traumatic brain injury have not been thoroughly studied. In this context, vinpocetine (VPN), derived from Vinca minor, exhibits notable anti-inflammatory and antioxidant properties. VPN is known for its neuroprotective role and is generally utilized for treating various neurodegenerative disorders. However, the function of VPN after cold-induced TBI needs to be studied in more detail. This study aims to investigate the neuroprotective effects of VPN at varying doses (5 mg/kg or 10 mg/kg) after cold-induced TBI. C57BL/6 mice were sacrificed 2 or 28 days after cold-induced TBI. Results indicate that VPN administration significantly reduces brain infarct volume, brain swelling, blood-brain barrier disruption, and DNA fragmentation in a dose-dependent manner. Additionally, VPN enhances neuronal survival in the ipsilesional cortex. In the long term, VPN treatment (5 mg/kg/day or 10 mg/kg/day, initiated 48 h post-TBI) improved locomotor activity, cell proliferation, neurogenesis, and decreased whole brain atrophy, specifically motor cortex atrophy. We performed liquid chromatography-tandem mass spectrometry (LC-MS/MS) to elucidate the underlying mechanisms to profile proteins and signaling pathways influenced by prolonged VPN treatment post-TBI. Notably, we found that 192 different proteins were significantly altered by VPN treatment, which is a matter of further investigation for the development of therapeutic targets. Our study has shown that VPN may have a neuroprotective role in cold-induced TBI.
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Registered trials
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