ArticleInflammation2023
Specific Activation of CB2R Ameliorates Psoriasis-Like Skin Lesions by Inhibiting Inflammation and Oxidative Stress.
Article in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Dental pulp stem cell-derived exosomes attenuate psoriatic inflammation by restoring epithelial redox homeostasis via a miR-1246/miR-17-3p-GPX2-NF-κB axis.Stem cell research & therapy · 2026Article
- Aloesin alleviates imiquimod-induced psoriasis in dermal layers through inhibition of interleukins and NF-κB signaling pathways.Scientific reports · 2025Article
- PDE4 inhibitors in psoriasis therapy: current insights and future directions.Inflammopharmacology · 2025Review
- Inflammaging and Immunosenescence in the Post-COVID Era: Small Molecules, Big Challenges.ChemMedChem · 2025Review
- The Effect of Phytocannabinoids and Endocannabinoids on Nrf2 Activity in the Central Nervous System and Periphery.Neurology international · 2024Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psoriasis is a chronic inflammatory skin disease. Inflammation and oxidative stress play crucial roles in the pathogenesis of psoriasis. Cannabinoid receptor type 2 (CB2R) is an attractive target for treating various inflammatory disorders. However, the precise role and mechanism of CB2R activation in psoriasis remain to be further elucidated. In this study, imiquimod (IMQ)-induced experimental psoriasis mice and tumor necrosis factor-α (TNF-α)-activated keratinocytes (HaCaT) were used to examine the effect of CB2R activation on psoriasis-like lesions and the mechanism in vivo and in vitro. Our results demonstrated that activation of CB2R by the specific agonist GW842166X (GW) significantly ameliorated IMQ-induced psoriasiform skin lesions in mice by reducing epidermal thickness and decreasing plaque thickness. On the one hand, GW alleviated inflammation by decreasing inflammatory cytokines and abating inflammatory cell infiltration. On the other hand, this treatment reduced the level of iNOS and downregulated the expression of CB2R in psoriatic skin tissue. Further studies suggested that the Kelch-like ECH-associated protein 1/nuclear factor erythroid-2-related factor (Keap1/Nrf2) signaling pathway might be involved. Our findings reveal that selective activation of CB2R may serve as a new strategy for the treatment of psoriasis.
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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.