ArticleNeurochemical research2017
L-PGDS Mediates Vagus Nerve Stimulation-Induced Neuroprotection in a Rat Model of Ischemic Stroke by Suppressing the Apoptotic Response.
Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Effect and Safety of Transcutaneous Auricular Vagus Nerve Stimulation on Recovery of Upper Limb Motor Function in Subacute Ischemic Stroke Patients: A Randomized Pilot Study.Neural plasticity · 2020Trial
- Review
- Mechanism and Applications of Vagus Nerve Stimulation.Current issues in molecular biology · 2025Review
- A narrative review of vagus nerve stimulation in stroke.Journal of central nervous system disease · 2024Review
- Research hotspots and frontiers of vagus nerve stimulation in stroke: a bibliometric analysis.Frontiers in neuroscience · 2024Review
- Mechanisms of Vagus Nerve Stimulation in Improving Motor Dysfunction After Stroke.Neuropsychiatric disease and treatment · 2024Review
- Lipocalin-type prostaglandin D synthase: a glymphopathy marker in idiopathic hydrocephalus.Frontiers in aging neuroscience · 2024Article
- Vagus Nerve Stimulation in Ischemic Stroke.Current neurology and neuroscience reports · 2023Review
- The Effects of Vagus Nerve Stimulation on Animal Models of Stroke-Induced Injury: A Systematic Review.Biology · 2023Review
- Vagus nerve stimulation is a potential treatment for ischemic stroke.Neural regeneration research · 2023Article
- USP10 is a potential mediator for vagus nerve stimulation to alleviate neuroinflammation in ischaemic stroke by inhibiting NF-κB signalling pathway.Frontiers in immunology · 2023Article
- Efficacy and safety of transcutaneous auricular vagus nerve stimulation combined with conventional rehabilitation training in acute stroke patients: a randomized controlled trial conducted for 1 year involving 60 patients.Neural regeneration research · 2022Article
- Vagus nerve stimulation alleviated cerebral ischemia and reperfusion injury in rats by inhibiting pyroptosis via α7 nicotinic acetylcholine receptor.Cell death discovery · 2022Article
- Non-invasive Vagus Nerve Stimulation in Cerebral Stroke: Current Status and Future Perspectives.Frontiers in neuroscience · 2022Review
- Protective Effect of Low-Dose Alcohol Consumption against Post-Ischemic Neuronal Apoptosis: Role of L-PGDS.International journal of molecular sciences · 2021Article
- Targeting the Autonomic Nervous System for Risk Stratification, Outcome Prediction and Neuromodulation in Ischemic Stroke.International journal of molecular sciences · 2021Review
- Vagal Nerve Stimulation Protects Against Cerebral Ischemia-Reperfusion Injury in Rats by Inhibiting Autophagy and Apoptosis.Neuropsychiatric disease and treatment · 2021Article
- The innate immune system and neurogenesis as modulating mechanisms of electroconvulsive therapy in pre-clinical studies.Journal of psychopharmacology (Oxford, England) · 2020Review
- Treadmill training improves neurological deficits and suppresses neuronal apoptosis in cerebral ischemic stroke rats.Neural regeneration research · 2019Article
- Effect of Electrical Vagus Nerve Stimulation on Cerebral Blood Flow and Neurological Outcome in Asphyxial Cardiac Arrest Model of Rats.Neurocritical care · 2019Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of lipocalin prostaglandin D2 synthase (L-PGDS) in brain ischemia has not been fully clarified to date. Vagus nerve stimulation (VNS) protects against cerebral ischemia/reperfusion (I/R) injury, but the mechanisms involved need further exploration. This study investigated the role of L-PGDS in cerebral I/R and whether this process was involved in the mechanism of VNS-mediated neuroprotection. Male Sprague-Dawley rats were pretreated with a lentiviral vector (LV) through intracerebroventricular injection, followed by middle cerebral artery occlusion (MCAO) and VNS treatment. The expression of L-PGDS in the peri-infarct cortex was examined. The localization of L-PGDS was determined using double immunofluorescence staining. Neurologic scores, infarct volume and neuronal apoptosis were evaluated at 24 h after reperfusion. The expression of apoptosis-related molecules was measured by western blot analysis. The expression of L-PGDS in the peri-infarct cortex increased at 12 h, reached a peak at 24 h after reperfusion, and lasted up to 3 days. VNS treatment further enhanced the expression of L-PGDS following ischemic stroke. L-PGDS was mainly expressed in neurons in the peri-infarct cortex. I/R rats treated with VNS showed better neurological deficit scores, reduced infarct volume, and decreased neuronal apoptosis as indicated by the decreased levels of Bax and cleaved caspase-3 as well as increased levels of Bcl-2. Strikingly, the beneficial effects of VNS were weakened after L-PGDS down-regulation. In general, our results suggest that L-PGDS is a potential mediator of VNS-induced neuroprotection against I/R injury.
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Registered trials
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 OpenQuestion graph.