ArticlePloS one2011
Clopidogrel, a P2Y12 receptor antagonist, potentiates the inflammatory response in a rat model of peptidoglycan polysaccharide-induced arthritis.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 51 citations in OpenAlex.
- Clopidogrel use is associated with an increased prevalence of Parkinson's disease, particularly among US adults with diabetes.Clinical parkinsonism & related disorders · 2026Article
- Chronic systemic inflammation by peptidoglycan-polysaccharide induces skeletal muscle atrophy in male and ovariectomized C57BL/6J mice.Physiological reports · 2025Article
- Electroacupuncture Alleviates Pain by Suppressing P2Y12R-Dependent Microglial Activation in Monoarthritic Rats.Neurochemical research · 2024Article
- The diversity and clinical implications of genetic variants influencing clopidogrel bioactivation and response in the Emirati population.Human genomics · 2024Article
- Differential effects of clopidogrel and/or aspirin on the healing of tooth extraction wound bone tissue.Frontiers in physiology · 2024Article
- Article
- The Signaling Pathway of the ADP Receptor P2YInternational journal of molecular sciences · 2023Review
- Clopidogrel-Associated Migratory Inflammatory Polyarthritis.The American journal of case reports · 2019Article
- The role of P2YCellular and molecular life sciences : CMLS · 2019Review
- Long-term Treatment with Anti-platelet Agents for Collagen-induced Arthritis Improves Radiological Findings.Osong public health and research perspectives · 2017Article
- The Inflammatory Role of Platelets: Translational Insights from Experimental Studies of Autoimmune Disorders.International journal of molecular sciences · 2016Review
- P2Y12 Receptor Modulates Sepsis-Induced Inflammation.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- P2Y12 antagonist attenuates eosinophilic inflammation and airway hyperresponsiveness in a mouse model of asthma.Journal of cellular and molecular medicine · 2016Article
- Platelets are relevant mediators of renal injury induced by primary endothelial lesions.American journal of physiology. Renal physiology · 2015Article
- CD39 improves survival in microbial sepsis by attenuating systemic inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Clopidogrel enhances periodontal repair in rats through decreased inflammation.Journal of clinical periodontology · 2014Article
- LPS-induced systemic inflammation is more severe in P2Y12 null mice.Journal of leukocyte biology · 2014Article
- The role of P2Y₁₂ receptor and activated platelets during inflammation.Current drug targets · 2014Review
- Prasugrel metabolites inhibit neutrophil functions.The Journal of pharmacology and experimental therapeutics · 2013Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The P2Y12 receptor plays a crucial role in the regulation of platelet activation by several agonists, which is irreversibly antagonized by the active metabolite of clopidogrel, a widely used anti-thrombotic drug. In this study, we investigated whether reduction of platelet reactivity leads to reduced inflammatory responses using a rat model of erosive arthritis. We evaluated the effect of clopidogrel on inflammation in Lewis rats in a peptidoglycan polysaccharide (PG-PS)-induced arthritis model with four groups of rats: 1) untreated, 2) clopidogrel-treated, 3) PG-PS-induced, and 4) PG-PS-induced and clopidogrel-treated. There were significant differences between the PG-PS+clopidogrel group when compared to the PG-PS group including: increased joint diameter and clinical manifestations of inflammation, elevated plasma levels of pro-inflammatory cytokines (IL-1 beta, interferon (IFN) gamma, and IL-6), an elevated neutrophil blood count and an increased circulating platelet count. Plasma levels of IL-10 were significantly lower in the PG-PS+clopidogrel group compared to the PG-PS group. Plasma levels of platelet factor 4 (PF4) were elevated in both the PG-PS and the PG-PS+clopidogrel groups, however PF4 levels showed no difference upon clopidogrel treatment, suggesting that the pro- inflammatory effect of clopidogrel may be due to its action on cells other than platelets. Histology indicated an increase in leukocyte infiltration at the inflammatory area of the joint, increased pannus formation, blood vessel proliferation, subsynovial fibrosis and cartilage erosion upon treatment with clopidogrel in PG-PS-induced arthritis animals. In summary, animals treated with clopidogrel showed a pro-inflammatory effect in the PG-PS-induced arthritis animal model, which might not be mediated by platelets. Elucidation of the mechanism of clopidogrel-induced cell responses is important to understand the role of the P2Y12 receptor in inflammation.
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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.