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. Author manuscript; available in PMC: 2013 May 2.
Published in final edited form as: Cell Metab. 2012 May 2;15(5):675–690. doi: 10.1016/j.cmet.2012.04.003

Figure 1. Improved mitochondrial function and increased mitochondrial biogenesis in response to resveratrol treatment requires SIRT1.

Figure 1

(A) Mitochondrial membrane potential and (B) ATP content in C2C12 cells treated with 25 μM resveratrol and 10 μM EX-527 for 24h.

(C) Representative immunoblot for SIRT1 and tubulin in C2C12 cells infected with SIRT1 or non-targeting shRNA.

(D) Mitochondrial membrane potential and (E) ATP content in C2C12 cells infected with SIRT1 or non-targeting shRNA and treated with 25 μM resveratrol for 24h.

(F) Mitochondrial DNA content analyzed by means of quantitative PCR in C2C12 cells treated with 10 μM EX-527 or (G) infected with SIRT1 or non-targeting shRNA and treated with 25 μM resveratrol. Relative expression values were normalized to untreated cells.

(H) C2C12 cells infected with SIRT1 or non-targeting shRNA, and expressing Flag-HA-PGC-1α were treated with resveratrol 25 μM for 24h and PGC-1α acetylation was tested in Flag immunoprecipitates. Total PGC-1α was evaluated on total extracts as input.

(I) PGC-1α, NRF-1, NDUFS8, SDHb, Uqcrc1, COX5b, ATP5a1 mRNA analyzed by means of quantitative RT-PCR in C2C12 cells infected with SIRT1 or non-targeting shRNA after 24h treatment with 25 μM resveratrol. Relative expression values were normalized to untreated cells.

Values are expressed as mean ± SEM. (*p < 0.05 versus DMSO).