Fig. 6

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-GSK3β and GSK3β (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 PPARα 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)