Fig 1: HucMDEs improve glucose and lipid metabolism both in vivo and in vitro. Glycolysis-related proteins (GCK, PFK, and PK) (a), glycogen synthesis-related proteins (p-GSK3ß, GSK3ß) (b), and gluconeogenesis-related proteins (G-6-P, PEPCK) (c) in the livers of the indicated groups were detected by Western blotting. d PAS staining in the livers of the indicated groups. e The hepatic lipid synthesis protein, SREBP-1c, and lipolytic protein, PPARa, in the livers of the indicated groups were detected by Western blotting. Glycolysis-related proteins (GCK, PFK, PK) (f), glycogen synthesis-related proteins (p-GSK3ß, GSK3ß) (g), and gluconeogenesis-related proteins (G-6-P, PEPCK) (h) in L-O2 cell groups of Control + PBS, 0.25 mM PA + PBS, PA + HDEs (30 µg/ml), and PA + HucMDEs (30 µg/ml) were detected by Western blotting. i PAS staining in L-O2 cells. j The hepatic lipid synthesis protein, SREBP-1c, and lipolytic protein, PPARa, in L-O2 cells of the indicated groups were detected by Western blotting. All the results are expressed as the mean ± SD (*P < 0:05; **P < 0:01; ***P < 0.001)
Fig 2: HucMDEs improve the glucose and lipid metabolism by promoting autophagy. a L-O2 cells were treated with PA, PA + HucMDEs, PA + 3-MA, or PA+ HucMDEs + 3-MA. Protein levels of MAP 1LC3B were examined by Western blotting. Glycolysis-related proteins (GCK, PFK, PK) (b), glycogen synthesis-related proteins (p-GSK3ß, GSK3ß) (c), and gluconeogenesis-related proteins (G-6-P, PEPCK) (d) in L-O2 cells of the indicated groups were detected by Western blotting. e PAS staining of L-O2 cells in the indicated groups. f SREBP-1c and PPARa in L-O2 cells of the indicated groups were detected by Western blotting. All results are expressed as the mean ± SD (*P < 0:05; **P < 0:01; ***P < 0.001)
Fig 3: HucMDEs promote autophagy by activating AMPK in L-O2 cells. Protein levels of p-AMPK and AMPK in the livers (a) and L-O2 cells (b) of the indicated groups. c L-O2 cells were transfected with AMPK siRNA or normal control (NC) siRNA and treated with HucMDEs for 48 h. p-AMPK, AMPK, BECN1, and MAP 1LC3B expression levels were examined by Western blotting. d Western blotting analysis of p-AMPK, AMPK, BECN1, and MAP 1LC3B treated with HucMDEs in the absence or presence of Comp C (the AMPK inhibitor, 20 µM) in L-O2 cells. Glycolysis-related proteins GCK, PFK, and PK (e); glycogen synthesis-related proteins p-GSK3ß and GSK3ß (f); and gluconeogenesis-related proteins G-6-P and PEPCK (g) in L-O2 cells of the indicated groups were detected by Western blotting. h PAS staining of the L-O2 cells. i SREBP-1c and PPARa in L-O2 cells of the indicated groups were detected by Western blotting. All the results were expressed as mean ± SD (*P < 0:05; **P < 0:01; ***P < 0.001)
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