Fig. 1

Epalrestat inhibits NLRP3 inflammasome activation in BMDMs and THP1 cells. A The structure of epalrestat. B Cell viability of BMDMs treated with epalrestat for 24 h as detected using a CCK-8 reagent. C LPS-primed BMDMs were treated with various doses of epalrestat for 1 h before stimulation with nigericin for 30 min. Immunoblot analysis of epalrestat was used to detect cleaved caspase-1 and IL-1β in the cell supernatants (Sup.) and the expression of NLRP3, caspase-1 p45, pro-IL-1β, and ASC in the cell lysates (Lys.). D–G The activity of caspase-1 D, secretion of IL-1β E, release of LDH F, and the production of TNF-α G in the Sup were assessed from samples described in C. H PMA-primed THP1 cells were treated with various doses of epalrestat for 1 h before stimulation with nigericin for 30 min. Immunoblot analysis of epalrestat was used to detect cleaved caspase-1 and IL-1β in the Sup and the expression of NLRP3, caspase-1 p45, pro-IL-1β, and ASC in the Lys. I–L The activity of caspase-1 I, secretion of IL-1β J, release of LDH K, and the production of TNF-α L in the Sup were assessed from samples described in H. Data are presented as the mean ± SD from at least three biological samples. Statistical differences were analyzed using an unpaired Student’s t-test. *P < 0.05, **P < 0.01, ***P < 0.001; ns not significant