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. 2022 Mar 8;13:859723. doi: 10.3389/fphar.2022.859723

FIGURE 7.

FIGURE 7

PF activated the AMPK/SIRT1/PGC-1α signaling pathway in C2C12 myoblasts induced by TNF-α. (A) Representative immunoblots using antibodies against p-AMPKα (Thr172), AMPKα, SIRT1, PGC-1α and GAPDH. (B) Quantification of protein expression. (C) The mRNA level of PGC-1α was assessed with RT–qPCR. (D) Cytotoxicity of Compound C (0, 2.5, 5, 7.5, 10, 12.5 and 15 μM) for 24 h (n = 6). (E) Cytotoxicity of EX-527 (0, 5, 10, 15, 20, 25 and 30 μM) for 24 h (n = 6). (F) The effect of different concentrations of Compound C on p-AMPKα/AMPKα protein levels. (G) The effect of different concentrations of EX-527 on SIRT1 protein inhibition. * p < 0.05, ** p < 0.01, *** p < 0.001 compared with the compound or EX-527 0 μM group. (H) Representative immunoblots using antibodies against MAFbx, MuRF-1, p-AMPKα (Thr172), AMPKα, SIRT1, PGC-1α and GAPDH. (I, J) Quantification of protein expression. All protein expression was normalized to that of GAPDH as a loading control. The data are presented as the means ± S.D. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001 compared with the Control group. # p < 0.05, ## p < 0.01, ### p < 0.001 compared with the TNF-α 40 ng/ml group, & p < 0.05, && p < 0.01, &&& p < 0.001 compared with the TNF-α 40 ng/ml + PF 50 μM group.