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. 2022 Sep 25;13(2):678–693. doi: 10.1016/j.apsb.2022.09.014

Figure 1.

Figure 1

COS inhibits NLRP3 inflammasome activation. (A) BMDMs were primed with LPS for 3 h and stimulated with ATP for 0.5 h after treatment with 5 μmol/L natural products library (119 compounds) for 0.5 h, ELISA of IL-1β in culture supernatant (SN). (B) Structure of COS. (C–E) LPS-primed BMDMs were treated with or without COS in different doses for 0.5 h and then stimulated with ATP for 0.5 h. Western blotting analysis of cleaved IL-1β and p20 levels in culture SN and pro-IL-1β, pro-caspase-1, and β-actin in lysates (Input) of BMDMs (C). IL-1β (D) or TNF-α (E) production was assessed using ELISA in SN. (F) BMDMs were primed with LPS for 3 h and then stimulated with ATP for 0.5 h after treatment with various doses of COS (1, 2, and 5 μmol/L) for 0.5 h. Western blotting analysis of GSDMD, or cleaved-GSDMD in lysates. (G) Assay of LDH release in the culture supernatants of LPS-primed BMDMs treated with different doses of COS for 0.5 h and then stimulated with ATP for 1 h. (H) ELISA of IL-1β in SN of PBMCs isolated from three healthy donors, treated with various doses of COS for 30 min, and then stimulated with LPS for 16 h. (I, J) LPS-primed BMDMs were treated with or without COS (2 μmol/L) for 0.5 h and then stimulated with ATP for 0.5 h, nigericin for 0.5 h, or Alum for 4 h. Western blotting analysis of mature IL-1β and p20 levels in SN (I) or ELISA of IL-1β production in SN (J). Data are presented as the mean ± SEM, n = 3; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001; ns, not significant.