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Normal brain function normally involves very small amounts of COX-1, however after brain damage, many cell types quickly produce COX-2, the responsive variant.COX2 is activated by pro-inflammatory stimuli and has been implicated as a defense reacting to glutamate imbalance, preferably in neurons

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S-glutathionylation of cysteine residues on NLRP3 [87] or in inflammasome-associated components caspase-1 [88], NEK-7 (NIMA-related kinase-7) [89] and the linker protein ASC [90], serves to suppress NLRP3 activity