Figure 1

Plasma and hepatic OPN expression is increased in response to liver I–R and the OPN deficiency increased hepatic I–R injury. Wt (n=8–10) and Opn^−/− (Opn^−/−) (n=5) mice underwent ischemia for 45 min followed by 4 h of reperfusion. SHAM controls (n=4–6) underwent the same procedure but without vascular occlusion. (a) The plasma level of OPN was evaluated before and after I–R in Wt mice. (b) Hepatic expression of OPN was evaluated in I–R lobes from Wt mice (Wt I–R) versus SHAM mice. (c) The plasma level of ALT and AST was evaluated before and after I–R in Wt, Opn^−/− and in SHAM mice. Results were expressed as means±S.E.M. Data were statistically analyzed using the Mann–Whitney test. *versus before I–R (a) or SHAM (b and c); ^$versus Wt I–R (c). P<0.05. (d) H&E staining of liver samples from Wt, Opn^−/− after I–R and SHAM mice. Typical pictures are shown. Dotted lines and arrows limit areas of necrosis; PT indicates portal triad; CLV indicates centrolobular vein. (e) The TUNEL assay was performed on liver sections as described in the Materials and Methods section. The liver sections were then counterstained with hematoxylin. Typical pictures are shown. (f) The level of caspase 3 activity was evaluated from a total lysate of control and I–R lobes from Wt (Wt Ctr; Wt I–R) (n=7), Opn^−/− (Opn^−/− Ctr; Opn^−/− I–R) (n=5) and SHAM mice (n=5). Results were expressed as means±S.E.M. Data were statistically analyzed using the Mann–Whitney test. ^≠versus SHAM, ^#versus Wt Ctr and *versus Opn^−/− Ctr. P<0.05