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

Table 1 Sequence of the cell-permeable PN50 peptide.

NF-kB p50 NLS-Cell-Permeable Motif

VQRKRQKLMPC-CRQIKIWFQNRRMKWKK

Sequences are given in single letter amino acid code. Underlined residues constitute the cell-permeable peptide penetratin.

Table 2 Histological scoring system for the evaluation of CCK-induced acute pancreatitis.

	0	0.5	1	1.5	2
Edema	Absent	Focal<50%	Diffuse>50%
Vascular Change	Absent	Congestion	Focal hemorrhage	Diffuse hemorrhage	Vascular necrosis or thrombosis
Inflammation	Absent	Focal/mild	Diffuse>50%
Acinar necrosis	Absent	Single acinar cell necrosis/foci of peripheral lobular damage	Lobular necrosis in 10% to 30% of the surface area	Lobular necrosis in 30% to 50% of the surface area	Lobular necrosis in >50% of the surface area/microabscesses
Calcification	Absent	Present
Fat necrosis	Absent	Present

The slides were coded and read for the traditional histological markers of pancreatic tissue injury by two independent observers who were blind to the experimental protocol. Semi-quantitative grading of interstitial edema, inflammation, hyperemia, and necrosis of acinar cells were evaluated in each animal, with the scoring system of Hughes et al[53].

Table 3 Effects of PN50 before and after treatment on the histologic parameters in CCK-induced acute pancreatitis (mean±SD).

	Group PS	Group CCK	Group PN50+CCK	Group CCK+PN50
Edema	0.1±0.067	0.955±0.045b	0.55±0.117bd	0.636 ± 0.097bd
Vascular Change	0.1±0.067	0.773± 0.079b	0.4±0.1ad	0.55 ± 0.05bc
Inflammation	0	0.591±0.061b	0.3±0.082bd	0.35 ± 0.076bc
Acinar necrosis	0	0.955±0.081b	0.45±0.09bd	0.65 ± 0.076bc
Calcification	0	0.125±0.065	0	0
Fat necrosis	0	0.167±0.071a	0.05±0.05	0.05±0.05

^aP<0.05,

^bP<0.01 vs group PS;

^cP<0.05,

^dP<0.01 vs group CCK.