A nuclear import inhibitory peptide ameliorates the severity of cholecystokinin-induced acute pancreatitis

Figure 1 Experimental protocol of CCK-induced acute pancreatitis.

Figure 2 PN50 suppresses transcriptional activity of NF-κB in TNF-α-stimulated L929 fibroblasts (A) and LPS-activated RAW 264. 7 macrophages (B) in vitro.

Figure 3 In vivo delivery of the NF-κB p50 NLS with penetratin into the pancreas (A) and lung (B).

Figure 4 Effect of PN50 on the pancreatic weight/body weight ratio (pw/bw) (A) and serum amylase activity (B) in CCK-induced acute pancreatitis. ^bP<0.01 vs group PS; ^dP<0.01 vs group CCK.

Figure 5 Effect of PN50 on the pancreatic (A) and lung (B) myeloperoxidase (MPO) activity and pancreatic TNF-α (C) and IL-6 (D) levels in CCK-induced acute pancreatitis. ^aP<0.05, ^bP<0.01 vs group PS; ^cP<0.05, ^dP<0.01 vs group CCK.

Figure 6 Effect of PN50 treatment on the pancreatic malondialdehyde (MDA) (A) and reduced glutathione (GSH) levels (B) in CCK-induced acute pancreatitis. ^bP<0.01 vs group PS; ^cP<0.05, ^dP<0.01 vs group CCK.

Figure 7 Effect of PN50 on pancreatic NF-κB binding activity in CCK-induced acute pancreatitis. A: a representative EMSA for pancreatic NF-κB DNA binding activity; B: the intensities of NF-κB bands. ^aP<0.05, ^bP<0.01 vs group PS; ^dP<0.01 vs group CCK.

Figure 8 Effect of PN50 on pancreatic morphological damage in CCK-induced pancreatitis. A: group PS (control group): normal pancreas (HE ×100); B: group CCK: marked edema, inflammatory activity, stasis (HE ×100); microfocal necroses, vacuolar degenerations in the acinar cells (insert: HE ×250); C: group PN50+CCK: mild inflammation, mild edema, fairly maintained parenchymal structure (HE ×100); mild degenerative changes in the acini (insert: HE ×250); D: group CCK+PN50: mild edema, minimal inflammatory activity (HE ×100); degenerative changes with apoptotic cells (arrows) in the acini (insert: HE ×250).