Mechanism Of Rat Cardiomyocyte Injury And Apoptosis Induced By Saturated Fatty Acid

Recently, Lipid accumulation in the heart has been observed under conditions of elevatedplasma free fatty acids, such as Type 2 diabetes mellitus and is linked with cardiomyocyte apoptosis. It isalso found that apoptosis can be induced by saturated fatty acid in cultured cell. In order to study themechanism of myocardial injury by saturated fatty acid, in first part of this study we got type 2 diabetic ratsby HFD-fed and STZ-treated, and observed metabolic disorder, cardiomyocyte apoptosis and heart functionof diabetic rats. At the same time diabetic rats were treated by metabolic drug L-CN. We found that plasmalipid level was increased followed by augment of FAT/CD36 on cardiomyocyte membrane, cardiomyocyteapoptosis, degresion of heart function, and L-CN showed significantly protective effect. For furtherstudying saturated fatty acid induced injury, we cultured neonatal rat cardiomyocytes with palmitate ofdifferent concentration. Significant effect of palmitate induced cardiomyocyte apoptosis was found, whitchcould be aggravated by CPT-1 inhibitor perhexiline and be lessened by CPT-1 cofactor L-CN. Previousstudies show ER stress occurs in palmitate-treated pancreaticβcell, therefore the effect of ER stress inpalmitate-induced cardiomyocyte apoptosis was approached in part 3 of this study. The results indicatedthat ER stress contributed to palmitate-induced cardiomyocyte apoptosis.