Table 1.

NOD-like receptor pyrin domain containing 3 inflammasome inhibitors investigated in the context of diabetic wound healing

Inhibitor	Mechanism	Study Type	Reference
Glyburide	Closure of potassium channel	In vitro, in vivo	36,47
Tranilast	NLRP3 NACHT domain binding	In vivo, clinical	48–50
YVAD	NF-κB activity limitation	In vitro, in vivo	36,50
MCC950	NLRP3–ASC oligomerization blocking	In vitro, in vivo	51–53
Bay 11-7082	NLRP3 NACHT domain binding	In vitro, in vivo	41,45,54
PPAR agonists	NF-κB activity limitation	In vitro, in vivo	55,56
ON1O1	Limitation of NF-κB activity, ROS, NLRP3–ASC oligomerization and potassium efflux	In vitro, in vivo, clinical	57–59
Metformin	NF-κB activity limitation and ROS inhibition	In vitro, in vivo	61–64
DPP-4 inhibitors	ROS inhibition	In vivo, clinical	65–70
Heparan sulfate	NLRP3 and ASC downregulation	In vitro, in vivo	71–73

ASC, apoptosis-associated speck-like protein; DPP-4, dipeptidyl peptidase 4; NF-κB, nuclear factor kappa B; NLRP3, NOD-like receptor pyrin domain containing 3; PPAR, peroxisome proliferator-activated receptor; ROS, reactive oxygen species.