Figure 6
(a). Representative photomicrographs of six experiments (hematoxylin and eosin staining, magnification × 400) demonstrating vacuolization (*) and hypereosinophillia (arrows) in kidneys from C57BL/6 mice 24 h after being subjected sham-operation or to liver ischemia reperfusion after vehicle- or sphinganine-1-phosphate treatment (0.1 mg/kg i.v. immediately before reperfusion and 0.2 mg/kg s.c. 2 h after reperfusion). Photographs are representative of six independent experiments. (b). Summary of renal injury scores (scale 0–3) for renal cortical vacuolization, peritubular leukocyte margination, proximal tubule simplification, and renal tubular hypereosinophilia for kidneys from mice subjected to liver IR after vehicle or sphinganine-1-phosphate treatment. Some mice were pretreated with PD98059 (PD, an inhibitor of MEK1 to inhibit ERK phosphorylation, 1 mg/kg, i.p., N=6) or with wortmannin (Wort, an inhibitor of PI3K to inhibit Akt phosphorylation, 1 mg/kg, i.p., N=6) 20 min before vehicle or sphinganine-1-phosphate treatment. Some mice were pretreated with pertussis toxin (PTX, 25 μg/kg, i.p.) 48 h before sphinganine-1-phosphate treatment. Mice pretreated with PD98059, wortmannin, or pertussis toxin showed increased indices of renal injury. *P<0.05 vs vehicle-treated IR group. #P<0.05 vs sphinganine-1-phosphate-treated hepatic IR group.
