Quantum Molecular Resonance Inhibits NLRP3 Inflammasome/Nitrosative Stress and Promotes M1 to M2 Macrophage Polarization: Potential Therapeutic Effect in Osteoarthritis Model In Vitro
Teresa Paolucci,
Vanessa Pino,
Osama Elsallabi,
Marialucia Gallorini,
Gianantonio Pozzato,
Alessandro Pozzato,
Paola Lanuti,
Victor Machado Reis,
Mirko Pesce,
Andrea Pantalone,
Roberto Buda,
Antonia Patruno
Affiliations
Teresa Paolucci
Department of Oral, Medical and Biotechnological Sciences, Physical Medicine and Rehabilitation, University G. D’Annunzio, 66100 Chieti, Italy
Vanessa Pino
Department of Medicine and Aging Sciences, University “G. d’Annunzio” of Chieti-Pescara, 66100 Chieti, Italy
Osama Elsallabi
Department of Medicine and Aging Sciences, University “G. d’Annunzio” of Chieti-Pescara, 66100 Chieti, Italy
Marialucia Gallorini
Department of Pharmacy, University “G. d’Annunzio” of Chieti-Pescara, 66100 Chieti, Italy
This study aimed to investigate the anti-inflammatory effects of Quantum Molecular Resonance (QMR) technology in an in vitro model of osteoarthritis-related inflammation. The study used THP-1-derived macrophages stimulated with lipopolysaccharide and hyaluronic acid fragments to induce the expression of inflammatory cytokines and nitrosative stress. QMR treatment inhibited COX-2 and iNOS protein expression and activity and reduced NF-κB activity. Furthermore, QMR treatment led to a significant reduction in peroxynitrite levels, reactive nitrogen species that can form during inflammatory conditions, and restored tyrosine nitration values to those similar to sham-exposed control cells. We also investigated the effect of QMR treatment on inflammasome activation and macrophage polarization in THP-1-derived macrophages. Results showed that QMR treatment significantly decreased NLRP3 and activated caspase-1 protein expression levels and downregulated IL-18 and IL-1β protein expression and secretion. Finally, our findings indicate that QMR treatment induces a switch in macrophage polarization from the M1 phenotype to the M2 phenotype.