Fig. 10

A schematic showing the effects of QSG on FA and glucose metabolism in HF induced by AMI. QSG exerted a remarkable regulatory effect on lipid metabolism by lowering serum levels of TC, TG and LDL-C. QSG activated FAT/CD36-CPT1-FAO signaling through upregulating the expressional levels of FAT/CD36, CPT1A, ACADL, ACADM, ACAA2 and SCP2, which would lead to an increase of FA uptake, transportation into mitochondria and β-oxidation. QSG promoted FA metabolism to a large extent on the up-regulation of transcriptional regulator PPARα, RXRα, RXRβ, RXRγ and PGC-1α. LDHA and PDK4 involved in glycolysis and glucose oxidation were all down-regulated by treatment with QSG, indicating QSG inhibited uncoupling of glycolysis from glucose oxidation. QSG facilitated TAC and the transfer of ATP from mitochondria to cytoplasm by increasing the protein levels of CKMT2 and SUCLA2. Moreover, the mitochondrial function was enhanced with QSG administration proved by the increased PGC-1α and the decreased UCP2