ArticleWorld journal of emergency medicine2021
Effects of extracellular vesicles from mesenchymal stem cells on oxygen-glucose deprivation/reperfusion-induced neuronal injury.
Article in World journal of emergency medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Extracellular Vesicles as Therapeutic Strategy for Ischemic Stroke.Journal of neurochemistry · 2025Review
- Stem cell-derived extracellular vesicles: novel therapeutics for cerebral injury following cardiac arrest and potential mechanisms.Cell & bioscience · 2025Review
- Beyond the hype: re-evaluating efficacy metrics and modeling rigor for MSC-EVs-based therapy in acute brain injury.Frontiers in medicine · 2025Review
- Protective Role of TRPC3 Gene Polymorphism (rs10518289) in Obstructive Sleep Apnea Hypopnea Syndrome Among Hypertensive Patients.Medical science monitor : international medical journal of experimental and clinical research · 2024Article
- Protective effect of mesenchymal stem cell-derived exosomal treatment of hippocampal neurons against oxygen-glucose deprivation/reperfusion-induced injury.World journal of emergency medicine · 2022Article
- Timing of brain computed tomography for predicting neurological prognosis in comatose cardiac arrest survivors: a retrospective observational study.World journal of emergency medicine · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSmall extracellular vesicles (sEVs) from bone marrow mesenchymal stem cells (BMSCs) have shown therapeutic potential for cerebral ischemic diseases. However, the mechanisms by which BMSC-derived sEVs (BMSC-sEVs) protect neurons against cerebral ischemia/reperfusion (I/R) injury remain unclear. In this study, we explored the neuroprotective effects of BMSC-sEVs in the primary culture of rat cortical neurons exposed to oxygen-glucose deprivation and reperfusion (OGD/R) injury.
methodsThe primary cortical neuron OGD/R model was established to simulate the process of cerebral I/R
resultsBMSC-sEVs (20 μg/mL, 40 μg/mL) significantly decreased the reactive oxygen species (ROS) productions, and increased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx). Additionally, BMSC-sEVs prevented OGD/R-induced neuronal apoptosis
conclusionsThese results demonstrate that BMSC-sEVs have significant neuroprotective effects against OGD/R-induced cell injury by suppressing oxidative stress and apoptosis, and Ca
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Registered trials
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