UDCA improves hepatic mitochondria biogenesis and dysfunction in ob/ob mice. Normal and ob/ob mice were treated with or without 50 mg/kg UDCA for 14 days. (A) Immunohistochemical staining analysis of SIRT1 and PGC-1α in the liver. Red arrow highlights the positive staining. Scale bars, 200 µm. (B) Western blot analysis of SIRT1 and PGC-1α protein levels in liver. qRT-PCR analysis of (C) Sirt1, Pgc-1α, Tfam, (D) Complex I, II, III, IV, V, (E) p22phox, p47phox, Nox2, and Nox4 mRNA expression in liver. Relative mRNA expression was normalized to Gapdh and then normalized to the controls. In all panels, results are expressed as the mean ± S.E.M. of five independent experiments, and statistical significance of differences between means was assessed using an unpaired Student’s t-test (* p ≤ 0.05; normal vs. ob/ob. #
p ≤ 0.05; ob/ob vs. ob/ob + UDCA). SIRT1, nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase sirtuin-1; PGC-1α, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; Tfam, mitochondrial transcription factors A; Nox, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase.