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. 2021 Jan 25;6(2):e134601. doi: 10.1172/jci.insight.134601

Figure 3. Echinatin does not directly target the ASC oligomerization and does not block K+ efflux or mitochondrial damage.

Figure 3

(A–C) LPS-primed BMDMs were pretreated with echinatin (40 μM) or vehicle and then stimulated with nigericin, poly(dA:dT), and Lfn-FliC — or Pam3CSK4-primed BMDMs were pretreated with echinatin (40 μM) or vehicle and then stimulated with transfected LPS. Cleaved caspase-1 and production of IL-1β were examined by IB analysis (A), and activity of caspase-1 (B) and secretion of IL-1β (C) in SN were assessed. (D) IB analysis of cross-linked ASC in the Triton X–insoluble pellet from LPS-primed BMDMs pretreated with echinatin (40 μM) or vehicle and then stimulated with nigericin, poly(dA:dT), Lfn-FliC, or Pam3CSK4-primed BMDMs were pretreated with echinatin (40 μM) or vehicle and then stimulated with transfected LPS. (E) Qualification of intracellular potassium in LPS-primed BMDMs pretreated with indicated dose of echinatin and stimulated with nigericin. (F) Staining with MitoTracker red in LPS-primed BMDMs pretreated with echinatin (40 μM) or vehicle and then stimulated with nigericin. Scale bar: 5 μm. Data are expressed as mean ± SEM (n = 3/group, resulting from 3 independent experiments). Statistics differences were analyzed by unpaired t test (B and C) or 1-way ANOVA followed by Dunnett’s post hoc test (E). **P < 0.01, ***P < 0.001.