Research Paper Volume 13, Issue 16 pp 20534—20551

NLRP3 inflammasome activation contributes to the pathogenesis of cardiocytes aging

NLRP3 inflammasomes were activated in the cardiocytes aging model induced by D-gal. H9c2 cells were treated with different concentrations of D-gal (0, 2, 10 and 50 g/L) for 24 hours. (A) Representative confocal fluorescent images showed that D-gal treatment increased the colocalization of NLRP3 (red) and caspase-1 (green) proteins in a concentration-dependent manner. (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.

Figure 2. NLRP3 inflammasomes were activated in the cardiocytes aging model induced by D-gal. H9c2 cells were treated with different concentrations of D-gal (0, 2, 10 and 50 g/L) for 24 hours. (A) Representative confocal fluorescent images showed that D-gal treatment increased the colocalization of NLRP3 (red) and caspase-1 (green) proteins in a concentration-dependent manner. (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.