NLRP3 and Hyperglycemia: Hyperglycemia induced redox perturbation by upregulating TXNIP protein expression and downregulating thioredoxin protein expression in DC, which was mitigated by H2S. H2S inhibited NLRP3 inflammasome activation in DC, whereas PAG (an inhibitor of CSE) counteracted the above protective effects of exogenous H2S. Overall, exogenous H2S alleviated myocardial inflammation by suppressing NLRP3 inflammasome activation in diabetic rats, which needs to be further demonstrated using NLRP3 inhibitors [48].