ZLN005 protects cardiomyocytes against high glucose-induced cytotoxicity by promoting SIRT1 expression and autophagy.

摘要: Diabetic cardiomyopathy increases the risk for development of heart failure independent coronary artery disease and hypertension. Either type 1 or 2 diabetes is often accompanied by varying degrees hyperglycemia, which has been proven to induce myocardial apoptosis in animal models. Recently, a novel small molecule, ZLN005, reported show antidiabetic efficacy mouse model, possibly induction PGC-1α expression. In this study, we investigated whether ZLN005 protects cardiomyocytes against high glucose-induced cytotoxicity mechanisms involved. Neonatal were incubated with media containing 5.5 33mM glucose 24h presence absence ZLN005. treatment led ameliorated cardiomyocyte oxidative injury, enhanced cell viability, reduced environment. Western blot analysis revealed that suppressed autophagy, whereas increased expression autophagy marker proteins ATG5, beclin1, LC3 II/LC3 I; increase was SIRT1. Furthermore, EX527, SIRT1-specific inhibitor, weakened protective effects on subjected glucose. Taken together, these results suggest suppresses injury promoting SIRT1 autophagy.