Skip to main content
. 2003 Oct 1;112(7):989–998. doi: 10.1172/JCI17970

Figure 6.

Figure 6

Hepatic ROS production and apoptosis induced by Fas agonist are suppressed by Stat3-C via Ref-1. LacZ, Stat3-C:LacZ, and Stat3-C:AdFer (Stat3-C:Fer) mice were infected with AdLacZ only, AxCAS3-C:AdLacZ (1:1), and AxCAS3-C:AdFer (1:1), respectively. Total amounts of adenovirus vectors were adjusted to 3 × 108 PFU/mouse in all experiments. (a) Immunoblots of Ref-1 and Stat3 proteins showing that AxCAS3-C increased Stat3 and Ref-1 proteins, but AdFer reduced them. Ref-1 protein was, however, expressed even in the liver of LS3-KO mice. (b) Superoxide generation assay and hydrogen peroxide assay in liver tissue*P < 0.05 vs. LacZ, **P < 0.05 vs. LacZ/Fas agonist, ***P < 0.05 vs. Stat3-C:LacZ/Fas agonist. Casp inh; i.e. Z-VAD-fmk. (c) Apoptotic cell death was quantitatively analyzed by ELISA. *P < 0.01 vs. LacZ, **P < 0.05 vs. LacZ/Fas agonist, ***P < 0.05 vs. Stat3-C:LacZ/Fas agonist. (d) Enzyme activity assays of caspase-3 and caspase-8. *P < 0.05 vs. LacZ/Fas agonist. All data are expressed as mean ± SEM (n = 5). RLU, relative light unit.