ArticleNaunyn-Schmiedeberg's archives of pharmacology2017
Cannabinoid receptor agonist WIN55,212-2 and fatty acid amide hydrolase inhibitor URB597 ameliorate neuroinflammatory responses in chronic cerebral hypoperfusion model by blocking NF-κB pathways.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Cannabinoid receptor agonist WIN 55,212-2 modulates systemic inflammatory and oxidative stress responses in streptozotocin-induced diabetic rats.Inflammopharmacology · 2026Article
- Selective autophagy inhibition alleviates oxidative stress-associated neurodegeneration in an AD+CCH model.Frontiers in aging neuroscience · 2026Article
- Autophagy Regulation Attenuates Neuroinflammation and Cognitive Decline in an Alzheimer's Disease Mouse Model with Chronic Cerebral Hypoperfusion.Inflammation · 2025Article
- Article
- CB1 Receptor Activation Provides Neuroprotection in an Animal Model of Glutamate-Induced Excitotoxicity Through a Reduction of NOX-2 Activity and Oxidative Stress.CNS neuroscience & therapeutics · 2024Article
- Mitigating neurodegenerative diseases: the protective influence of baicalin and baicalein through neuroinflammation regulation.Frontiers in pharmacology · 2024Review
- Neuroprotection and Beyond: The Central Role of CB1 and CB2 Receptors in Stroke Recovery.International journal of molecular sciences · 2023Review
- Human ESC-derived immunity- and matrix- regulatory cells ameliorated white matter damage and vascular cognitive impairment in rats subjected to chronic cerebral hypoperfusion.Cell proliferation · 2022Article
- The Cannabinoid Receptor Agonist, WIN-55212-2, Suppresses the Activation of Proinflammatory Genes Induced by Interleukin 1 Beta in Human Astrocytes.Cannabis and cannabinoid research · 2022Article
- The interplay between oxidative stress and autophagy: focus on the development of neurological diseases.Behavioral and brain functions : BBF · 2022Review
- Fatty Acid Amide Hydrolase (FAAH) Inhibition Modulates Amyloid-Beta-Induced Microglia Polarization.International journal of molecular sciences · 2021Article
- URB597 Prevents the Short-Term Excitotoxic Cell Damage in Rat Cortical Slices: Role of Cannabinoid 1 Receptors.Neurotoxicity research · 2021Article
- The Role of the Effects of Autophagy on NLRP3 Inflammasome in Inflammatory Nervous System Diseases.Frontiers in cell and developmental biology · 2021Review
- The Minocycline Ameliorated the Synaptic Plasticity Impairment in Vascular Dementia.Iranian journal of pharmaceutical research : IJPR · 2021Article
- The Cannabinoid Receptor Agonist WIN55,212-2 Ameliorates Hippocampal Neuronal Damage After Chronic Cerebral Hypoperfusion Possibly Through Inhibiting Oxidative Stress and ASK1-p38 Signaling.Neurotoxicity research · 2020Article
- Cannabinoid-mediated Modulation of Oxidative Stress and Early Inflammatory Response after Hypoxia-Ischemia.International journal of molecular sciences · 2020Article
- URB597 protects against NLRP3 inflammasome activation by inhibiting autophagy dysfunction in a rat model of chronic cerebral hypoperfusion.Journal of neuroinflammation · 2019Article
- Resveratrol Activates Autophagy via the AKT/mTOR Signaling Pathway to Improve Cognitive Dysfunction in Rats With Chronic Cerebral Hypoperfusion.Frontiers in neuroscience · 2019Article
- Inhibition of excessive autophagy and mitophagy mediates neuroprotective effects of URB597 against chronic cerebral hypoperfusion.Cell death & disease · 2018Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
The present study explored the protective effects of cannabinoid receptor agonist WIN55,212-2 (WIN) and fatty acid amide hydrolase inhibitor URB597 (URB) against neuroinflammation in rats with chronic cerebral hypoperfusion (CCH). Activated microglia, astrocytes, and nuclear factor kappa B (NF-κB) p65-positive cells were measured by immunofluorescence. Reactive oxygen species (ROS) was assessed by dihydroethidium staining. The protein levels of cluster of differentiation molecule 11b (OX-42), glial fibrillary acidic protein (GFAP), NF-κB p65, inhibitor of kappa B alpha (IκB-a), IκB kinase a/β (IKK a/β), phosphorylated IKK a/β (p-IKK a/β), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF)-α, and interleukin-1β (IL-1β) were examined by western blotting or enzyme-linked immunosorbent assay. All the protein levels of OX-42, GFAP, TNF-a, IL-1β, COX-2, and iNOS are increased in CCH rats. WIN and URB downregulated the levels of OX-42, GFAP, TNF-α, IL-1β, COX-2 and iNOS and inhibited CCH-induced ROS accumulation in CCH rats, indicating that WIN and URB might exert their neuroprotective effects by inhibiting the neuroinflammatory response. In addition, the NF-κB signaling pathway was activated by CCH in frontal cortex and hippocampus, while the aforementioned changes were reversed by WIN and URB treatment. These findings suggest that WIN and URB treatment ameliorated CCH-induced neuroinflammation through inhibition of the classical pathway of NF-κB activation, resulting in mitigation of chronic ischemic 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.