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. 2014 Mar 14;306(9):L816–L828. doi: 10.1152/ajplung.00323.2013

Fig. 4.

Fig. 4.

Effect of loss and gain of SIRT1 function on antioxidant genes and enzymes in mouse lungs exposed to CS. SIRT1+/−, SIRT1 Tg, and their WT littermates were exposed to CS for 3 days, and the mRNA levels of antioxidant genes were determined by RT-PCR in mouse lungs. CS exposure did not have any effect on the mRNA levels of CuZn superoxide dismutase (SOD) and MnSOD in lungs of WT mice. Neither SIRT1 deficiency nor overexpression changed the levels of CuZnSOD mRNA in mouse lungs regardless of air or CS exposure. The levels of MnSOD mRNA were reduced in SIRT1+/− mice, whereas SIRT1 genetic overexpression increased MnSOD mRNA compared with the corresponding WT littermates. Gel pictures shown are representative of at least 3 separate mice. The reassembly of noncontiguous gel lanes is demarcated by white spaces clearly (A). Real-time PCR showed that the mRNA levels of CuZnSOD, MnSOD, and NADPH quinone oxidoreductase-1 (NQO-1) were decreased in SIRT1+/− mice (B) compared with WT mice, and these effects were augmented by SIRT1 transgenic overexpression (C). MnSOD activity was decreased in SIRT1+/− mice, which was increased in SIRT1 Tg mice compared with WT mice in response to CS exposure (D). Data are shown as means ± SE (n = 3 to 6 per group). *P < 0.05 vs. the corresponding air-exposed mice; +P < 0.05, ++P < 0.01 vs. the WT mice. HO-1, heme oxygenase-1.