Pancreas-specific RelA/p65 truncation increases susceptibility of acini to inflammation-associated cell death following cerulein pancreatitis
J. Clin. Invest. Hana Algül, et al. 117:1490 doi:10.1172/JCI29882 [Go to this article.]

Figure 3
Pancreas-specific truncation of RelA/p65 exacerbates AP. (A) rela^flox/flox and rela^Δ/Δ mice were given 8 hourly i.p. injections of cerulein (50 μg/kg) and sacrificed 8, 12, or 24 hours after the first injection. Histological sections of rela^flox/flox and rela^Δ/Δ mice were analyzed at the indicated time points. Note the increased vacuolization, morphologically apoptotic cells, ghost cells, edema, infiltration, and massive necrosis in the rela^Δ/Δ pancreata. (B) Pancreatic injury was determined by measuring amylase and LDH enzyme activity in serum. Total tissue homogenates were obtained from pancreata of cerulein-injected mice at the indicated time points and subjected to trypsin activity analysis. Pancreatic edema was determined indirectly by increase in pancreatic weight. (C) H&E-stained pancreas sections from rela^flox/flox and rela^Δ/Δ mice 24 hours after cerulein-induced inflammation were used to measure and quantify necrotic parenchymal surface area. TUNEL assay results are expressed as the apoptotic index of pancreata from mice with AP. Apoptotic cells exhibited black nuclei. (D) l-Arginine–induced pancreatitis was evaluated 72 hours after induction. Pancreata and lungs were removed for morphological analysis by H&E. Note the appearance of focal necrosis in the pancreata of both groups. (E) Serum was removed for amylase and lipase evaluation at the indicated time points. Note the significant release of amylase and lipase into the serum in rela^Δ/Δ mice. Lung inflammation was evaluated as described in Methods. Values are mean ± SD for independent animals (n = 5). *P < 0.05 versus rela^flox/flox. Original magnification, ×50 (A, inset); ×200 (A and D); ×100 (C, inset); ×100 (C).