ArticleCNS neuroscience & therapeutics2024
CB1 Receptor Activation Provides Neuroprotection in an Animal Model of Glutamate-Induced Excitotoxicity Through a Reduction of NOX-2 Activity and Oxidative Stress.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Pathological Roles of Astrocytes in Traumatic Brain Injury.CNS neuroscience & therapeutics · 2026Review
- Radical Revelations: The Interplay of Nitrosative Stress, the Endocannabinoid System, and Treatment of Age-Related Disorders.International journal of molecular sciences · 2026Review
- Neuroprotective effects of cobalt oxide nanoparticles through mitigating oxidative stress and reactive glial responses in traumatic brain injury.Materials today. Bio · 2025Article
- Cannabinoids and Extracellular Vesicles as Potential Biomarkers and Therapeutic Targets in Neuropsychiatric Disorders: A Hypothesis-Driven Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Wuling San ameliorates cerebral ischemia-reperfusion injury via suppression of the TRPM2/NLRP3 pathway.European journal of medical research · 2025Article
- Cannabinoid Receptors Reduced Early Brain Damage by Regulating NOX-2 and the NLRP3 Inflammasome in an Animal Model of Intracerebral Hemorrhage.CNS neuroscience & therapeutics · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
backgroundExcitotoxicity is a process in which NADPH oxidase-2 (NOX-2) plays a pivotal role in the generation of reactive oxygen species (ROS). Oxidative stress influences the expression of Aquaporin 4 (AQP4), a water channel implicated in blood-brain barrier (BBB) permeability and edema formation. The endocannabinoid system is widely distributed in the brain, particularly through the cannabinoid receptor type 1 (CB1) and type 2 (CB2), which have been shown to have a neuroprotective function in brain injury. Given the significant involvement of NOX-2 in ROS production during excitotoxicity, our research aims to assess the participation of NOX-2 in the neuroprotective effect of the cannabinoid receptor agonist WIN55,212-2 against glutamate-induced excitotoxicity damage in the striatum using in vivo model.
methodsWild-type mice (C57BL/6) and NOX-2 KO (gp91
resultsThe activation of the endocannabinoid receptors demonstrated a neuroprotective response during excitotoxicity, meditated by NOX-2. The reduction in ROS production led to a decrease in neuroinflammation, and AQP4 expression, resulting in reduced edema formation, and BBB permeability.
conclusionsDuring excitotoxic damage, WIN55,212-2 inhibits NOX-2-induced ROS production, reducing brain 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 Socratic graph.