ArticleJournal of stroke2021
Neuroprotective Effects of GV1001 in Animal Stroke Model and Neural Cells Subject to Oxygen-Glucose Deprivation/Reperfusion Injury.
Article in Journal of stroke, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- GV1001 reduces pathological 4R tau and functional deficits in models relevant to progressive supranuclear palsy.Scientific reports · 2026Article
- Transcriptomic and functional annotation datasets for GV1001 peptide treatment in an experimental autoimmune encephalomyelitis mouse model.Data in brief · 2026Article
- Neuroprotective effects of curcumin, memantine, and caffeic acid in a Rat model of cerebral ischemia-reperfusion injury.Frontiers in pharmacology · 2026Article
- Molecular imaging of stem cell therapies in ischemic stroke.European journal of nuclear medicine and molecular imaging · 2025Review
- GV1001 reduces neurodegeneration and prolongs lifespan in 3xTg-AD mouse model through anti-aging effects.Aging · 2024Article
- MicroRNA Regulation for Inflammasomes in High Glucose-Treated ARPE-19 Cells.Journal of ophthalmology · 2024Article
- Exploring the Causal Relationship Between Telomere Biology and Alzheimer's Disease.Molecular neurobiology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
background and purposePrevious studies have revealed the diverse neuroprotective effects of GV1001. In this study, we investigated the effects of GV1001 on focal cerebral ischemia-reperfusion injury (IRI) in rats and oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury in neural stem cells (NSCs) and cortical neurons.
methodsFocal cerebral IRI was induced by transient middle cerebral artery occlusion (MCAO). Brain diffusion-weighted imaging (DWI) was performed 2 hours after occlusion, and a total of 37 rats were treated by reperfusion with GV1001 or saline 2 hours after occlusion. Fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging, immunohistochemistry, and neurobehavioral function analyses were performed. Additionally, OGD/R-injured NSCs and cortical neurons were treated with different GV1001 concentrations. Cell viability, proliferation, migration, and oxidative stress were determined by diverse molecular analyses.
resultsIn the stroke model, GV1001 protected neural cells against IRI. The most effective dose of GV1001 was 60 μM/kg. The infarct volume on FLAIR 48 hours after MCAO compared to lesion volume on DWI showed a significantly smaller ratio in the GV1001-treated group. GV1001-treated rats exhibited better behavioral functions than the saline-treated rats. Treatment with GV1001 increased the viability, proliferation, and migration of the OGD/R-injured NSCs. Free radicals were significantly restored by treatment with GV1001. These neuroprotective effects of GV1001 have also been demonstrated in OGD/R-injured cortical neurons.
conclusionsThe results suggest that GV1001 has neuroprotective effects against IRI in NSCs, cortical neurons, and the rat brain. These effects are mediated through the induction of cellular proliferation, mitochondrial stabilization, and anti-apoptotic, anti-aging, and antioxidant effects.
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