Astragalus polysaccharide liposome nanoparticles mediate fatty acid translocase (FAT)/CD36 to improve fatty acid metabolism and regulate glucocorticoid receptor levels in diabetic cardiomyopathy

Abnormal myocardial metabolism is the leading cause of diabetic cardiomyopathy (DCM). Astragalus polysaccharide (APS) combination with liposome nanoparticles (APS-nano) exhibits greater efficacy. Therefore, this study assessed regulatory effect of APS-nano on fatty acid translocase (FAT)/CD36. Fifty SD rats were assigned into control group, model group, APS group, APS-nano group, and FAT/CD36 inhibitor group ( n =10, each group), followed by analysis of FAT/CD36 mRNA, protein levels, and glucocorticoid receptor expression. APS-nano group rats had highest level of insulin among all groups and lowest blood sugar. The content of Total cholesterol (TC), triglyceride (TG) and Free Fatty Acid (FFA) in APS-nano group was lower than APS and model groups ( P = 0.000), with higher TC and FFA than control group ( P <0.001), while insulin, blood sugar, TC, TG and FFA in the APS group were lower than model group ( P = 0.000). FAT/CD36 mRNA in the model, APS, and APS-nano groups decreased to varying degrees ( P <0.01). Administration of APS-nano greatly increased glucocorticoid receptor ( P <0.01). APS-nano can regulate FAT/CD36 expression and improve fatty acid metabolism, thereby lowering myocardial tissue metabolism and inhibiting glucocorticoid receptor levels.