aPC ameliorates inflammasome activation after myocardial IRI. (A) Experimental design. (B-C) aPC treatment reduces infarct size. Representative heart sections showing infarcted area detected by triphenyl tetrazolium chloride staining (area encircled by dashed line; size bar, 20 µm) (B) and dot plot summarizing data (C). (D-I) aPC pretreatment significantly reduces cardiac Nlrp3 expression and cleavage of caspase-1 (cl-Casp1) and IL-1β (cl–IL-1β). Representative immunoblots (glyceraldehyde-3-phosphate dehydrogenase [GAPDH]: loading control [cont]) (D) and bar graph summarizing data (E). Arrowheads indicate inactive (white) and active (black) forms of caspase-1 or IL-1β (D). The active form was quantified (E). aPC treatment reduces caspase-1 activity within infarcted area. Representative images of frozen sections incubated with FLICA-Casp1 probes (size bar, 20 µm) (F) and dot plot summarizing data (G). aPC reduces plasma IL-1β (H) and IL-18 levels (I) after myocardial IRI; dot plots summarizing data. Sham-operated mice (sham) or mice with myocardial IRI without (cont; PBS) or with aPC pretreatment (aPC). Data shown represent mean ± SEM of at least 6 mice per group. *P < .05, **P < .01; analysis of variance (C,E,H,I) or Mann-Whitney U test (G).