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. Author manuscript; available in PMC: 2024 Mar 15.
Published in final edited form as: Cell Rep. 2024 Jan 23;43(2):113700. doi: 10.1016/j.celrep.2024.113700

Figure 3. AA inhibits the NLRP3 inflammasome.

Figure 3.

(A and B) IL-1β production in LPS-primed BMDMs after 1 h stimulation with 10 μM nigericin with or without 40 μM AA added after priming (A) or during priming (B).

(C-F) Cellular viability (C and E) and IL-1β (D and F) produced by LPS-primed WT BMDMs after stimulation with nigericin (10 μM, 1 h) (C and D) or ATP (5 mM, 30 min) (E and F) in presence of 40 μM AA.

(G-I) Cellular viability (G), ASC speck quantification (H), and IL-1β (I) produced by WT BMDMs primed with Pam3CSK4 (200 ng/mL, 4 h) after stimulation with palmitic acid (PA; 1 mM, 16 h) in presence of 40 μM AA.

(J-L) Cellular viability (J), ASC speck quantification (K), and IL-1β (L) produced by THP-1 cells (differentiated with PMA, 200 ng/mL for 24 h followed by 24 h washout) primed with Pam3CSK4 (200 ng/mL, 4 h) after stimulation with PA (500 μM, 24 h) in presence of 40 μM AA.

*p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001 (one-way analysis of variance with Tukey’s multiple comparison test or Student’s unpaired t test). n.s., not significant. Data are from at least three independent experiments (mean and SEM).