Fig. 6
mAb A treatment prevents the accumulation of branched chain amino acids (BCAA) post-MI via enhancing their catabolism. a Myocardial BCAA concentration, b representative blots for BCAA catabolism enzymes, c mitochondrial branched chain aminotransferase (BCATm)/α-tubulin, d Krüppel-like factor 15 (KLF15)/α-tubulin, e phosphorylated p38 mitogen-activated protein kinases (p-p38 MAPKThr180/Tyr182)/p38 MAPK, f phosphorylated-transforming growth factor beta-activated kinase 1 (p-TAK1 Thr184/187)/TAK1. Densitometry were carried out when protein bands were normalised to α-tubulin bands for intra-experiment variation. Data are reported as mean ± SEM n = 6/group. S sham, V vehicle, Ab mAb A, MI myocardial infarction