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. 2019 Jul 17;20(14):3502. doi: 10.3390/ijms20143502

Figure 4.

Figure 4

Genetic deletion of Ephx2 or pharmacological inhibition of sEH inhibited IR-induced nucleotide-binding oligomerization domain-like receptor (NLR) family pyrin domain containing 3 (NLRP3) inflammasome formation and activation. Representative immunoblots and densiometric quantification of the expression of the cytosolic proteins (A) sEH and (B) NLRP3 in mice hearts after 30 min ischemia and 40 min reperfusion. All expressions were normalized to glyceraldehyde 3-phosphate dehydrogenase (GAPDH) loading control. (C) Cardiac caspase-1 enzymatic activity assessed in the cytosolic fraction following 30min ischemia and 40min reperfusion. The assay quantitated the fluorescence intensity resulting from the cleavage of the caspase-1 specific fluorogenic substrate Ac-YVAD-AMC by the cytosolic heart homogenates. (D) Cardiac IL-1β protein levels assessed by enzyme-linked immunosorbent assay (ELISA) in the cytosolic fraction following 30 min ischemia and 40 min reperfusion. Values represent mean ± SEM, * p < 0.05 vs. WT Aerobic CT, ☨ p < 0.05 vs. sEH null Aerobic, # p < 0.05 vs. WT IR (n = 3–5 per group).