Figure 3. PLC and Ryr Are Required for Resveratrol to Activate AMPK.

(A) The phosphorylation of ACC and AMPK induced by resveratrol in C2C12 myotubes in the absence (–) or presence (+) of calcium chelator BAPTA-AM (20 μM). We used myotubes derived from low-passage (<10) C2C12 cells.

(B) The phosphorylation of ACC and AMPK induced by resveratrol in C2C12 myotubes in the absence (–) or presence (+) of the CamKK inhibitor STO609 (5 mg/ml) for 50 μM (left) or 300 μM (right) resveratrol. We used myotubes derived from low-passage (<10) C2C12 cells.

(C) The phosphorylation of ACC and AMPK induced by 007 in C2C12 myotubes in the absence (–) or presence (+) of the CamKK inhibitor STO609 (5 μg/ml). C2C12 cells of <10 passages were used.

(D) The increase in intracellular Ca²⁺ levels after resveratrol treatment (50 μM) in C2C12 myotubes loaded with Ca²⁺ indicator Fluo-4 AM in the presence of PLC inhibitor U73122 (20 μM). F indicates the fluorescence level and DF indicates the change in fluorescence (n = 3).

(E) The phosphorylation of ACC and AMPK induced by resveratrol (50 μM) in C2C12 myotubes in the absence (–) or presence (+) of the PLC inhibitor U73122 (20 μM).

(F) Phosphorylation of ACC and AMPK induced by resveratrol in C2C12 myotubes in the absence (–) or presence (+) of the Ryr inhibitor ryanodine.

(G) Resveratrol-induced phosphorylation of S2815 in Ryr2 in the presence of siRNA specific for Epac1 or control siRNA.

See also Figure S2.