Teneligliptin mitigates diabetic cardiomyopathy by inhibiting activation of the NLRP3 inflammasome

Figure 6 Teneligliptin prevented activation of the cardiac NLRP3 inflammasome and injury in cardiomyocytes. Primary cardiomyocytes were treated with high glucose (30 mmol/L) with or without teneligliptin (2.5 or 5 µM) for 24 h. A: Expression of NLRP3 and caspase-1 were measured by western blot assays; B: Levels of IL-1β as measured by ELISA; C: Levels of creatine kinase-MB and aspartate transaminase level. ^aP < 0.05 vs control group; ^bP < 0.05 vs high glucose 30 mmol/L group; ^cP < 0.05 vs high glucose 0 mmol/L + teneligliptin 0 µM group; ^dP < 0.05 vs high glucose 30 mmol/L + teneligliptin 0 µM group, n = 5. CK-MB: Creatine kinase-MB; AST: Aspartate transaminase; IL: Interleukin.