H2S also decreased the HG-induced endothelial injury and the protein expression level of NLRP3 inflammasome in vivo and in vitro, while the silencing of NLRP3 had the effect similar to that of H2S, suggesting that H2S protected against diabetes-accelerated atherosclerosis by inhibiting the activation of NLRP3 inflammasome 88. Here, NLRP3 is linked to diabetes mellitus.