Figure 3.
H2S influences NLRP3 inflammasome through signal 1 and signal 2. Signal 1 is mediated by microbial ligands recognized by TLR which activates the NF-kB pathway to promote the protein expression level of pro-IL-1β and NLRP3. The signal 2 promotes the assembly of the NLRP3 inflammasome complex. Under noninfectious conditions, K+ efflux leads to the activation of NLRP3 inflammasome. Various endogenous and exogenous particulates, including uric acid crystal, promote lysosomal damage to activate NLRP3 inflammasome. Additionally, the increase of ROS level in the cell also activates the NLRP3 inflammasome. H2S can influence NLRP3 inflammasome through the above pathways. ASC: apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain; NF-kB: nuclear factor kappa-light-chain-enhancer of activated B cells; ROS: reactive oxygen species; TLR:toll-like receptor