ArticleBritish journal of pharmacology2011
Inhibition of COX-2 expression by endocannabinoid 2-arachidonoylglycerol is mediated via PPAR-γ.
Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.
- Cannabinoids, the Blood-Brain Barrier, and Neurodegeneration: Mechanisms, Dysregulation, and Therapeutic Perspectives.Biomolecules · 2026Pooled it
- Oral ibuprofen differentially affects plasma and sweat lipid mediator profiles in healthy adult males.Prostaglandins & other lipid mediators · 2018Trial
- Tissue-specific roles of monoacylglycerol (MAG) in metabolic diseases.Immunometabolism (Cobham, Surrey) · 2026Review
- Inhibition of endocannabinoid degradation in astrocytes reprograms glial reactivity and prevents seizure sequelae.Journal of neuroinflammation · 2026Article
- Cannabinoids in immune system-related diseases: From bench to clinic.Chinese medical journal · 2026Review
- Selective Inactivation of Astrocytic Monoacylglycerol Lipase for Alzheimer's Disease Therapy.bioRxiv : the preprint server for biology · 2025Article
- Cannabinoids: Role in Neurological Diseases and Psychiatric Disorders.International journal of molecular sciences · 2024Review
- Cannabigerol Mitigates Haloperidol-Induced Vacuous Chewing Movements in Mice.Neurotoxicity research · 2024Article
- Overabundant endocannabinoids in neurons are detrimental to cognitive function.bioRxiv : the preprint server for biology · 2024Article
- Cannabinoids' Role in Modulating Central and Peripheral Immunity in Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Monoacylglycerol Lipase Inhibition Prevents Short-Term Mitochondrial Dysfunction and Oxidative Damage in Rat Brain Synaptosomal/Mitochondrial Fractions and Cortical Slices: Role of Cannabinoid Receptors.Neurotoxicity research · 2023Article
- Exploring the role of COX-2 in Alzheimer's disease: Potential therapeutic implications of COX-2 inhibitors.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023Review
- Endocannabinoid control of neuroinflammation in traumatic brain injury by monoacylglycerol lipase in astrocytes.Neural regeneration research · 2023Article
- 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
- Endocannabinoid 2-Arachidonoylglycerol Synthesis and Metabolism at Neuronal Nuclear Matrix Fractions Derived from Adult Rat Brain Cortex.International journal of molecular sciences · 2023Article
- Inhibition of 2-arachidonoylglycerol degradation enhances glial immunity by single-cell transcriptomic analysis.Journal of neuroinflammation · 2023Article
- Plasma-Derived Exosomes from NAFLD Patients Modulate the Cannabinoid Receptors' Expression in Cultured HepaRG Cells.International journal of molecular sciences · 2023Article
- Endocannabinoid metabolism and Alzheimer's disease.Neural regeneration research · 2022Article
- Enhancing endocannabinoid signalling in astrocytes promotes recovery from traumatic brain injury.Brain : a journal of neurology · 2022Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeEndocannabinoids have both anti-inflammatory and neuroprotective properties against harmful stimuli. We previously demonstrated that the endocannabinoid 2-arachidonoylglycerol (2-AG) protects hippocampal neurons by limiting the inflammatory response via a CB(1) receptor-dependent MAPK/NF-κB signalling pathway. The purpose of the present study was to determine whether PPARγ, an important nuclear receptor, mediates 2-AG-induced inhibition of NF-κB phosphorylation and COX-2 expression, and COX-2-enhanced miniature spontaneous excitatory postsynaptic currents (mEPSCs). EXPERIMENTAL APPROACH: By using a whole-cell patch clamp electrophysiological recording technique and immunoblot analysis, we determined mEPSCs, expression of COX-2 and PPARγ, and phosphorylation of NF-kB in mouse hippocampal neurons in culture. KEY
resultsExogenous and endogenous 2-AG-produced suppressions of NF-κB-p65 phosphorylation, COX-2 expression and excitatory synaptic transmission in response to pro-inflammatory interleukin-1β (IL-1β) and LPS were inhibited by GW9662, a selective PPARγ antagonist, in hippocampal neurons in culture. PPARγ agonists 15-deoxy-Δ(12,14) -prostaglandin J(2) (15d-PGJ(2)) and rosiglitazone mimicked the effects of 2-AG on NF-κB-p65 phosphorylation, COX-2 expression and mEPSCs, and these effects were eliminated by antagonism of PPARγ. Moreover, exogenous application of 2-AG or elevation of endogenous 2-AG by inhibiting its hydrolysis with URB602 or JZL184, selective inhibitors of monoacylglycerol lipase (MAGL), prevented the IL-1β- and LPS-induced reduction of PPARγ expression. The 2-AG restoration of the reduced PPARγ expression was blocked or attenuated by pharmacological or genetic inhibition of the CB(1) receptor. CONCLUSIONS AND IMPLICATIONS: Our results suggest that CB(1) receptor-dependent PPARγ expression is an important and novel signalling pathway in endocannabinoid 2-AG-produced resolution of neuroinflammation in response to pro-inflammatory insults.
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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.