Hepatocyte cytoskeleton during ischemia and reperfusion - influence of ANP-mediated p38 MAPK activation

Figure 3 Effect of p38 MAPK inhibition on distribution of F- and G-actin. 20 min prior to ischemia livers were preconditioned with 200 nmol/L ANP or left untreated (Co) followed by 24-h ischemia at 4 °C. In different experiments, livers were perfused with SB203580 (2 μmol/L) or with a combination of SB203580 (2 μmol/L) and ANP (200 nmol/L). After ischemia livers were snap-frozen, homogenized and divided into cytoskeletal (A) and cytosolic (B) fraction by fractionation as described above. Samples were analyzed by Western blotting using an anti-actin antibody for detection of F-actin (A) in the cytoskeletal fraction and G-actin (B) in the cytosolic fraction. One representative Western blot is shown for each fraction. Bars show percentage of hepatic F-actin (A) or G-actin (B) in ANP, ANP+SB203580 and SB203580 treated livers referring to untreated control livers. Results are expressed as mean±SE of n = 4 experiments in each treatment group. ^bP<0.01 vs control after 24-h ischemia.