Research Paper Volume 13, Issue 16 pp 20534—20551

NLRP3 inflammasome activation contributes to the pathogenesis of cardiocytes aging

NAC inhibited NLRP3 inflammasomes in the cardiocytes aging model. H9c2 cells were pre-treated with or without NAC (1 mM), a commonly used ROS scavenger, for 1 hour and then incubated with or without 10 g/L D-gal for 24 hours. (A) Representative confocal fluorescent images showed that NAC 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 8. NAC inhibited NLRP3 inflammasomes in the cardiocytes aging model. H9c2 cells were pre-treated with or without NAC (1 mM), a commonly used ROS scavenger, for 1 hour and then incubated with or without 10 g/L D-gal for 24 hours. (A) Representative confocal fluorescent images showed that NAC 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.