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Hana Algül, Matthias Treiber, Marina Lesina, Hassan Nakhai, Dieter Saur, Fabian Geisler, Alexander Pfeifer, Stephan Paxian, Roland M. Schmid
Published in Volume 117, Issue 6
J Clin Invest. 2007; 117(6):1490–1501 doi:10.1172/JCI29882
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Figure 3
Pancreas-specific truncation of RelA/p65 exacerbates AP.

(A) relaflox/flox and relaΔ/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 relaflox/flox and relaΔ/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 relaΔ/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 relaflox/flox and relaΔ/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 relaΔ/Δ mice. Lung inflammation was evaluated as described in Methods. Values are mean ± SD for independent animals (n = 5). *P < 0.05 versus relaflox/flox. Original magnification, ×50 (A, inset); ×200 (A and D); ×100 (C, inset); ×100 (C).