Sulforaphane attenuates activation of NLRP3 and NLRC4 inflammasomes but not AIM2 inflammasome

• Sulforaphane blocks NLRP3 and NLRC4 inflammasomes but not AIM2 inflammasome.
• Sulforaphane attenuates the priming step of NLRP3 inflammasome.
• Sulforaphane inhibits generation of mitochondrial reactive oxygen species.

Sulforaphane (SFN), a compound within the isothiocyanate group of organosulfur compounds originating from cruciferous vegetables, has gained attention for its antioxidant, anti-inflammatory, and cancer chemopreventive properties. However, the effects of SFN on inflammasomes, which are multi-protein complexes that induce maturation of interleukin (IL)-1β, have been poorly studied. In this study, we investigated the effects of SFN on the assembly of NLRP3, NLRC4, and AIM2 inflammasomes as well as on the priming step of NLRP3 inflammasome in murine macrophages. In our results, SFN attenuated activation of NLRP3 and NLRC4 inflammasomes but not AIM2 inflammasome. In addition, SFN blocked expression of the NLRP3 gene and pro-IL-1β during the priming step. SFN further attenuated IL-1β secretion of monosodium uric acid-induced peritonitis in mice. Lastly, SFN inhibited generation of mitochondrial reactive oxygen species, which trigger NLRP3 inflammasome activation. Thus, SFN is suggested as an anti-inflammasome molecule for NLRP3 and NLRC4 inflammasome activation.