FIGURE 1
FROM:
Reduced acetaminophen-induced liver injury in mice by genetic disruption of IL-1 receptor antagonist
Takuya Ishibe, Akihiko Kimura, Yuko Ishida, Tatsunori Takayasu, Takahito Hayashi, Koichi Tsuneyama, Kouji Matsushima, Ikuhiro Sakata, Naofumi Mukaida and Toshikazu Kondo
BACK TO ARTICLEFigure 1.
(a) The susceptibility of hepatocytes isolated from WT and IL-1ra KO mice to APAP or NAPQI. Hepatocytes were isolated from WT and IL-1ra KO mice, and cultured in the presence of APAP (5 mM) or NAPQI (400 
M) for 4 h, as described in 'Materials and Methods'. Each value represents mean
s.e.m. (n=6 animals). **
P<0.01, WT vs IL-1ra KO mice. (b) Western blotting analysis of APAP adducts in hepatocyte homogenates from WT and IL-1ra KO mice after APAP treatment. Representative results from six independent experiments are shown here. (c) Western blotting analysis of APAP adducts in the livers of WT and IL-1ra KO mice administered with APAP (100–300 mg/kg). Representative results from six independent experiments are shown here. (d) Blood acetaminophen concentrations in WT and IL-1ra KO mice after APAP challenge (200 mg/kg). Each value represents means.e.m. (n=6 animals). **
P<0.01, WT vs IL-1ra KO mice. (e) Intrahepatic GSH levels in WT and IL-1ra KO mice after APAP challenge (200 mg/kg). Each value represents means.e.m. (n=6 animals).
