Fig. 6

MaR1-induced Akt activation in hepatic I/R injury is dependent on ALXR. a Akt and p-Akt protein levels in mice with the treatment of PBS or MaR1 6 h after reperfusion. b The expression of Akt and p-Akt was evaluated by Western blot in the liver of the indicated group. c Western blot showing the protein levels of total and phosphorylated Akt in mice subjected to vehicle or Akt inhibitor administration with or without the treatment of MaR1. d Representative Western blotting and quantitative analyses revealing p-Akt protein expression in the liver of indicated groups. e Serum ALT levels were measured in WT mice treated with vehicle or Akt inhibitor in the presence or absence of MaR1and harvested 6 h after I/R (n =5-6 for I/R group). f Representative H&E images (original magnification ×20) of liver sections from WT mice treated with vehicle or Akt inhibitor in the presence or absence of MaR1and harvested 6 h post-reperfusion. g Percentages of necrotic areas are shown in the indicated I/R groups (n = 3). h Serum IL-6 levels of PBS- and MaR1-treated mice subjected to the vehicle or Akt inhibitor and harvested 6 h post-reperfusion as analyzed by ELISA (n = 5-6 for each group). i Cleaved-caspase 3 protein expression of PBS- and MaR1-treated mice subjected to the vehicle or Akt inhibitor and liver tissues harvested 6 h after I/R as analyzed by Western blotting. Data are presented as means± SEM. *P\(<\)0.05, **P\(<\) 0.01, ***P\(<\)0.001