Protective and Pain-Killer Effects of AMC3, a Novel N-Formyl Peptide Receptors (FPRs) Modulator, in Experimental Models of Rheumatoid Arthritis.
VEGF-A
cartilage
chondrocyte
disease modifying agent
inflammation
interleukin-1β
oxidative stress
pain
pharmacological modulator
rheumatoid arthritis
Journal
Antioxidants (Basel, Switzerland)
ISSN: 2076-3921
Titre abrégé: Antioxidants (Basel)
Pays: Switzerland
ID NLM: 101668981
Informations de publication
Date de publication:
02 Jun 2023
02 Jun 2023
Historique:
received:
03
05
2023
revised:
26
05
2023
accepted:
31
05
2023
medline:
28
6
2023
pubmed:
28
6
2023
entrez:
28
6
2023
Statut:
epublish
Résumé
Rheumatoid arthritis is an autoimmune disorder that causes chronic joint pain, swelling, and movement impairment, resulting from prolonged inflammation-induced cartilage and bone degradation. The pathogenesis of RA, which is still unclear, makes diagnosis and treatment difficult and calls for new therapeutic strategies to cure the disease. Recent research has identified FPRs as a promising druggable target, with AMC3, a novel agonist, showing preclinical efficacy in vitro and in vivo. In vitro, AMC3 (1-30 µM) exhibited significant antioxidant effects in IL-1β (10 ng/mL)-treated chondrocytes for 24 h. AMC3 displayed a protective effect by downregulating the mRNA expression of several pro-inflammatory and pro-algic genes (iNOS, COX-2, and VEGF-A), while upregulating genes essential for structural integrity (MMP-13, ADAMTS-4, and COLIAI). In vivo, AMC3 (10 mg kg
Identifiants
pubmed: 37371936
pii: antiox12061207
doi: 10.3390/antiox12061207
pmc: PMC10295763
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : University of Florence
ID : na
Organisme : Ministry of University Education and Research (Ministero dell'Istruzione dell'Università e della Ricerca - MIUR)
ID : na
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