To explore the mechanism of Exenatide reduces the apoptosis of diabetic neonatal cardiomyocyte
We used a high glucose/palmitate intervention to mimic Type 2 diabetes in vitro. Neonatal cardiomyocytes were divided into control group(C); diabetes group (D), diabetes treated with Exenatide group(DE); diabetes and block the expression of APPL1 group(DB); diabetes treated with Exenatide and block the expression of APPL1 group (BE). We detected apoptosis rate of cardiomyocytes by TUNEL, the adiponectin levels by ELISA, and the protein expression of APPL1, p-AMPK/T-AMPK, PPARα, and NF-κB by western blotting.
Compared with those in the D group, the level of apoptosis in the C and DE groups was significantly decreased (P<0.05); the concentrations of adiponectin was significantly increased (P<0.05); the expression levels of APPL1, p-AMPK/T-AMPK, PPARα were significantly increased (P<0.05); and the expression levels of NF-κB were decreased (P<0.05). Compared with those in the DB group, the cardiomyocyte apoptosis rate was increased; the expression levels of APPL1, p-AMPK/T-AMPK, PPARα were decreased (P<0.05); the expression levels of NF-κB was significantly increased (P<0.05); and the concentrations of adiponectin was significantly decreased (P<0.05) in BE group.
After diabetic cardiomyocyte were treated with Exenatide, the concentrations of adiponectin was increased, the expression level of the APPL1-AMPK-PPARα axis was increased, and the expression of NF-κB and cardiomyocyte apoptosis rate were decreased, block the expression of APPL1 can reverse this effect.