ArticleThe Journal of biological chemistry2008
Endocannabinoid 2-arachidonoylglycerol protects neurons by limiting COX-2 elevation.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
66 citing papers in PubMed, 140 citations in OpenAlex.
- Inhibition of endocannabinoid degradation in astrocytes reprograms glial reactivity and prevents seizure sequelae.Journal of neuroinflammation · 2026Article
- Delta-9-tetrahydrocannabinol and Cannabidiol for Pain: Preclinical and Clinical Models.Current topics in behavioral neurosciences · 2026Review
- Selective Inactivation of Astrocytic Monoacylglycerol Lipase for Alzheimer's Disease Therapy.bioRxiv : the preprint server for biology · 2025Article
- Kaempferol Regulates Lipid Homeostasis, Endocannabinoid System, and PPARα in Rat Cerebral Cortex Following BCCAO/R.Biomolecules · 2025Article
- The antioxidant N-acetylcysteine prevents cortical neuropathological phenotypes caused by adolescent Δ-9-tetrahydrocannabinol exposure in male rats.Translational psychiatry · 2025Article
- [Effects of hyperoxia on the expression of hippocampal N-methyl D-aspartate receptor 1 and its synapse-associated molecules in neonatal rats].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Article
- Cannabinoids: Role in Neurological Diseases and Psychiatric Disorders.International journal of molecular sciences · 2024Review
- Overabundant endocannabinoids in neurons are detrimental to cognitive function.bioRxiv : the preprint server for biology · 2024Article
- Estrogen deprivation and estrogen receptor α antagonism decrease DSS colitis in female mice.Pharmacology research & perspectives · 2024Article
- Article
- Inhibiting degradation of 2-arachidonoylglycerol as a therapeutic strategy for neurodegenerative diseases.Pharmacology & therapeutics · 2023Review
- Augmentation of 2-arachidonoylglycerol signaling in astrocytes maintains synaptic functionality by regulation of miRNA-30b.Experimental neurology · 2023Article
- Inhibition of 2-arachidonoylglycerol degradation enhances glial immunity by single-cell transcriptomic analysis.Journal of neuroinflammation · 2023Article
- Endocannabinoid metabolism and Alzheimer's disease.Neural regeneration research · 2022Article
- TDP-43 drives synaptic and cognitive deterioration following traumatic brain injury.Acta neuropathologica · 2022Article
- Enhancing endocannabinoid signalling in astrocytes promotes recovery from traumatic brain injury.Brain : a journal of neurology · 2022Article
- Review
- Review
- Inhibition of 2-Arachidonoylglycerol Metabolism Alleviates Neuropathology and Improves Cognitive Function in a Tau Mouse Model of Alzheimer's Disease.Molecular neurobiology · 2021Article
- Confound, Cause, or Cure: The Effect of Cannabinoids on HIV-Associated Neurological Sequelae.Viruses · 2021Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Endocannabinoids are involved in synaptic signaling and neuronal protection; however, our understanding of the mechanisms by which endocannabinoids protect neurons from harmful insults remains elusive. 2-Arachidonoylglycerol (2-AG), the most abundant endogenous cannabinoid and a full agonist for cannabinoid receptors (CB1 and CB2), is a substrate for cyclooxygenase-2 (COX-2) and can be metabolized by COX-2. Here we show, however, that 2-AG is also capable of suppressing elevation of hippocampal COX-2 expression in response to proinflammatory and excitotoxic stimuli. 2-AG prevents neurodegeneration from toxic assaults that elevate COX-2 expression and inhibits the COX-2 elevation-enhanced excitatory glutamatergic synaptic transmission. The action of 2-AG on suppression of COX-2 appeared to be mediated via the pertussis toxin-sensitive G protein-coupled CB1 receptor and MAPK/NF-kappaB signaling pathways. Our results reveal that 2-AG functions as an endogenous COX-2 inhibitor protecting neurons from harmful insults by preventing excessive expression of COX-2, which provides a mechanistic basis for opening up new therapeutic approaches for protecting neurons from inflammation- and excitotoxicity-induced neurodegeneration.
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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.