Published online Apr 15, 2024. doi: 10.4239/wjd.v15.i4.724
Peer-review started: October 8, 2023
First decision: December 6, 2023
Revised: December 20, 2023
Accepted: February 27, 2024
Article in press: February 27, 2024
Published online: April 15, 2024
Processing time: 186 Days and 14.5 Hours
Diabetic cardiomyopathy (DCM), which is a complication of diabetes, poses a great threat to public health. Recent studies have confirmed the role of NLRP3 (NOD-like receptor protein 3) activation in DCM development through the infla
To examine the therapeutic effects of teneligliptin on DCM in diabetic mice.
Streptozotocin was administered to induce diabetes in mice, followed by trea
Marked increases in cardiomyocyte area and cardiac hypertrophy indicator heart weight/tibia length reductions in fractional shortening, ejection fraction, and heart rate; increases in creatine kinase-MB (CK-MB), aspartate transaminase (AST), and lactate dehydrogenase (LDH) levels; and upregulated NADPH oxidase 4 were observed in diabetic mice, all of which were significantly reversed by tene
Overall, teneligliptin mitigated DCM by mitigating activation of the NLRP3 inflammasome.
Core Tip: Teneligliptin mitigated diabetic cardiomyopathy by mitigating the activation of NLRP3 (NOD-like receptor protein 3) inflammasome. Teneligliptin reversal markedly increased cardiomyocyte area and heart weight/tibia length, reduced fractional shortening, ejection fraction, and heart rate, increased creatine kinase-MB (CK-MB), aspartate transaminase (AST), and lactate dehydrogenase (LDH) levels, and upregulated NADPH oxidase 4 in streptozotocin-induced diabetic mice. Teneligliptin repressed activated NLRP3 inflammasome and increased CK-MB, AST, and LDH levels in glucose-stimulated cardiomyocytes, accompanied by an upregulation of phosphorylated-adenosine 5‘-monophosphate and activated protein kinase.