Figure 1: Pharmacological inhibition of PKM2 impairs inflammasome activation.

LPS (500 ng ml⁻¹, 3 h)-primed mouse BMDMs and human PMA-differentiated THP1 cells were respectively treated with inflammasome activators (ATP (5 mM, 30 min), poly(dA:dT) (1 μg ml⁻¹, 8 h), MDP (200 ng ml⁻¹, 8 h) or flagellin (200 ng ml⁻¹, 8 h)) in the absence or presence of shikonin at the same time (1 and 5 μM). IL-1β, IL-18 and HMGB1 (a,b) in supernatants and caspase-1 activity (c) in whole-cell extract were assayed with ELISA or activity assay kit (n=3, *P<0.05, ANOVA LSD test). In parallel, the levels of IL-1β and cleaved caspase-1 (p20) in culture supernatants (SN) and the precursors of IL-1β (pro-IL-1β) and caspase-1 (pro-caspase-1) in lysates of BMDMs were assayed using western blot (d). As a control, the cationic lipid transfection reagent LyoVec did not induce the cleavage of IL-1β and caspase-1 in BMDMs. All quantification data expressed as means±s.e.m of three independent experiments. Western blot data are representative of two independent experiments.