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Cited by 29Pain Mechanisms and TreatmentsFibromyalgia and Chronic Fatigue Syndrome ResearchPain Management and Treatment

RETRACTED: Role of Etanercept and Infliximab on Nociceptive Changes Induced by the Experimental Model of Fibromyalgia

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Cordaro, Marika, Siracusa, Rosalba, D’Amico, Ramona, Genovese, Tiziana, Franco, Gianluca, Marino, Ylenia, Di Paola, Davide, Cuzzocrea, Salvatore +3 more·2022·International Journal of Molecular Sciences
DOI 10.3390/ijms23116139PMC PMC9181785
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Abstract

BACKGROUND: Fibromyalgia is a clinical condition that affects 1% to 5% of the population. No proper therapy has been currently found. It has been described that inflammation plays a central role in the nerve sensitizations that characterize the pathology. METHODS: This paper aimed to evaluate the efficacy of etanercept and infliximab in the management of pain sensitization. Fibromyalgia was induced by three injections once a day of reserpine at the dose of 1 mg/kg. Etanercept (3 mg/kg) and infliximab (10 mg/kg) were administered the day after the last reserpine injection and then 5 days after that. Behavioral analyses were conducted once a week, and molecular investigations were performed at the end of the experiment. RESULTS: Our data confirmed the major effect of infliximab administration as compared to etanercept: infliximab administration strongly reduced pain sensitization in thermal hyperalgesia and mechanical allodynia. From the molecular point of view, infliximab reduced the activation of microglia and astrocytes and the expression of the purinergic P2X7 receptor ubiquitously expressed on glia and neurons. Downstream of the P2X7 receptor, infliximab also reduced p38-MAPK overexpression induced by the reserpine administration. CONCLUSION: Etanercept and infliximab treatment caused a significant reduction in pain. In particular, rats that received infliximab showed less pain sensitization. Moreover, infliximab reduced the activation of microglia and astrocytes, reducing the expression of the purinergic receptor P2X7 and p38-MAPK pathway.

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Cited by

Sorted by citations

Authors
Cordaro, M., Siracusa, R., D’Amico, R., Genovese, T., Franco, G., Marino, Y., Di Paola, D., Cuzzocrea, S., Impellizzeri, D., Di Paola, R., & Fusco, R.
Affiliations
  • University of Messina (IT)
  • Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Viale Ferdinando Stagno D’Alcontres 31, 98166 Messina, Italy
  • Department of Veterinary Sciences, University of Messina, 98168 Messina, Italy
Corresponding author
  • Cuzzocrea, Salvatore
  • Impellizzeri, Daniela
ORCID
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2022-05-30
Volume
23
Issue
11
Pages
6139
ISSN
1422-0067 (ISSN-L)
DOI
10.3390/ijms23116139
PMC
PMC9181785
OpenAlex
W4281613679
Cited by
29
References
2
Citations by year
2026: 4 · 2025: 3 · 2024: 7 · 2023: 8 · 2022: 7
FWCI
3.87
Type
journal article
Language
en
Status
Retracted
Update notices
Open access
Licence
Locations
  • International Journal of Molecular Sciences (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Fibromyalgia and Chronic Fatigue Syndrome Research
  • Health Sciences › Medicine › Anesthesiology and Pain Medicine › Pain Management and Treatment
Keywords
fibromyalgia, etanercept, infliximab, pain sensitization, thermal hyperalgesia, mechanical allodynia, microglial activation, astrocyte activation, P2X7 receptor, p38 MAPK pathway, anti-TNF therapy
MeSH terms
Etanercept, Infliximab, Animals, Fibromyalgia, Hyperalgesia, Models, Theoretical, Pain, Reserpine, p38 Mitogen-Activated Protein Kinases, Rats, Nociception

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