Research Paper Volume 13, Issue 16 pp 20534—20551

NLRP3 inflammasome activation contributes to the pathogenesis of cardiocytes aging

MCC950 inhibited NLRP3 inflammasomes in the cardiocytes aging model induced by D-gal. H9c2 cells were pre-treated with or without MCC950 (10μM), a commonly used NLRP3 inhibitor, for 1 hour, and then incubated with or without 10g/L D-gal for 24 hours. (A) Representative confocal fluorescent images showed that MCC950 pre-treatment decreased the colocalization of NLRP3 (red) and caspase 1 (green) proteins in the cardiocytes aging model induced by D-gal. (B) Representative immunoblots of the NLRP3 and ASC proteins and the corresponding quantification were shown. (C) IL-1β, IL-18 and LDH release levels in cell culture were detected. NLRP3, Nod-like receptor family pyrin domain containing 3; ASC, apoptosis-associated speck-like protein.

Figure 5. MCC950 inhibited NLRP3 inflammasomes in the cardiocytes aging model induced by D-gal. H9c2 cells were pre-treated with or without MCC950 (10μM), a commonly used NLRP3 inhibitor, for 1 hour, and then incubated with or without 10g/L D-gal for 24 hours. (A) Representative confocal fluorescent images showed that MCC950 pre-treatment decreased the colocalization of NLRP3 (red) and caspase 1 (green) proteins in the cardiocytes aging model induced by D-gal. (B) Representative immunoblots of the NLRP3 and ASC proteins and the corresponding quantification were shown. (C) IL-1β, IL-18 and LDH release levels in cell culture were detected. NLRP3, Nod-like receptor family pyrin domain containing 3; ASC, apoptosis-associated speck-like protein.