Research Paper Volume 13, Issue 16 pp 20534—20551

NLRP3 inflammasome activation contributes to the pathogenesis of cardiocytes aging

Inhibition of NLRP3 by MCC950 attenuated cardiocytes aging induced by D-gal in H9c2 cells. 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 bright-field photomicrographs showed that MCC950 treatment decreased the percentage of cells expressing β-galactosidase. (B) Flow cytometry analysis was applied to detect the β-galactosidase mean fluorescence intensity after the MCC950 treatment. (C) The CellEvent™ Senescence Green staining showed that MCC950 treatment decreased the senescence-associated β-galactosidase expression induced by D-gal. (D) The aging-associated proteins (P53, P21) were detected by western blot, and the corresponding quantification was present.

Figure 4. Inhibition of NLRP3 by MCC950 attenuated cardiocytes aging induced by D-gal in H9c2 cells. 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 bright-field photomicrographs showed that MCC950 treatment decreased the percentage of cells expressing β-galactosidase. (B) Flow cytometry analysis was applied to detect the β-galactosidase mean fluorescence intensity after the MCC950 treatment. (C) The CellEvent™ Senescence Green staining showed that MCC950 treatment decreased the senescence-associated β-galactosidase expression induced by D-gal. (D) The aging-associated proteins (P53, P21) were detected by western blot, and the corresponding quantification was present.