Figure 3.

Normalizing mitochondrial function by cyclophilin D genetic ablation improves Arg-AP. Mice were subjected to Arg-AP, killed at 72 hours (A), 24 hours (C,E-G), or as indicated (B); and histopathologic changes (A; H&E staining) and pancreatitis responses (B-H) were measured. (C,D). Inflammatory infiltration was measured on pancreatic tissue immunostained for the neutrophil marker myeloperoxidase (MPO) and macrophage marker F4/80 (see also Supplementary Figure 7). (E,F). Pancreatic levels of phosphorylated and total p65/RelA (E) were measured by IB, and NF-κB DNA binding activity (F), by EMSA. In this and other figures, ERK1/2 or GAPDH are loading controls, and each lane on IB represents an individual animal. The narrow white space on EMSA gel indicates the lanes are on the same gel but not contiguous. (G,H). Subcellular localization of HMGB1 in pancreas was analyzed by IF using Volocity software. Scale bars: 10 μm. Values are mean ± SEM (n = 3–4). *P < .05 vs wt saline-treated mice; ^#P < .05 vs same treatment in CypD KO mice; ^$P < .05 vs saline-treated CypD KO mice.