Branched-Chain Amino Acid Supplementation Reduces Oxidative Stress and Prolongs Survival in Rats with Advanced Liver Cirrhosis
Figure 8
Effect of BCAA on JNK-FoxO1 pathway-mediated gluconeogenesis in cultured cells.
Cells were cultured with or without 2.4 mM of DEM for 2 h. Western blotting of p-c Jun, p-JNK and non-phosphorylated FoxO1 in the nuclear fraction, and p-FoxO1, PEPCK, G6P and β-actin in the cytoplasmic fraction of cultured cells (Fig. 8-A). Protein expression level of the p-c Jun was enhanced by DEM (n = 4), but was repressed by BCAA supplementation (n = 4) (Fig. 8-B). Protein expression of p-JNK was enhanced by DEM (n = 4), but it was repressed by BCAA supplementation (n = 4) (Fig. 8-C). Protein expression of FoxO1 was enhanced by DEM (n = 4), but it was repressed by BCAA supplementation (n = 4) (Fig. 8-D). The rate of FoxO1 to p-FoxO1 was elevated by DEM (n = 4), but it was repressed by BCAA supplementation (n = 4) (Fig. 8-E). Protein expression of PEPCK was enhanced by DEM (n = 4), but it was repressed by BCAA supplementation (n = 4) (Fig. 8-F). Protein expression of G6P was enhanced by DEM (n = 4), but it was repressed by BCAA supplementation (n = 4) (Fig. 8-G). DEM, diethylmaleate; BCAA, branched-chain amino acids; p-c Jun, phosphorylated c-Jun, p-JNK, phosphorylated c-Jun N-terminal kinase; FoxO1, forkhead box O1; p-FoxO1, phosphorylated forkhead box O1; PEPCK, phosphoenolpyruvate carboxykinase; G6P, glucose 6-phosphatase.