Fig. 5: NLRP3 inhibitor CRID3 or knockdown NLRP3 with si-RNA decreased pyroptosis and attenuated cardiac hypertrophy induced by TAC or Ang-II. | Cell Death Discovery

Fig. 5: NLRP3 inhibitor CRID3 or knockdown NLRP3 with si-RNA decreased pyroptosis and attenuated cardiac hypertrophy induced by TAC or Ang-II.

From: NLRP3-mediated pyroptosis aggravates pressure overload-induced cardiac hypertrophy, fibrosis, and dysfunction in mice: cardioprotective role of irisin

Fig. 5

A Immunoblots showing the protein levels of NLRP3 (A1, A2), ASC (A1, A3), cleaved caspase-1 (A1, A4), and GSDMD-N (A1, A5) in the cardiac tissue of indicated groups. B Percentage of TUNEL-positive cells in the indicated groups. C Proportion of heart to body weight in the indicated groups. D Quantification of the cross-sectional area of cardiomyocytes of the left ventricle in the indicated groups. E Quantification of the myocardial fibrosis in the indicated groups. F Quantitative analysis of left ventricular EF in the indicated groups. G Immunoblots showing protein levels of NLRP3 and ASC (G1, G2), cleaved caspase-1, and GSDMD-N (G1, G3) in the suitably treated cardiomyocytes. H Percentage of PI-positive cells in the suitably treated cardiomyocytes. I Measurement of the cell surface area of cardiomyocytes in the indicated groups. J mRNA expression of cardiac hypertrophy markers BNP and β-MHC in the suitably treated cardiomyocytes. Results are presented as the mean ± SEM, n = 6. ∗P < 0.01 compared to control, #P < 0.01 compared to TAC or Ang-II group. CRID3 (cytokine release inhibitory drug 3, NLRP3 inhibitor) known as CP-456773 or MCC950.

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