Journal
WORLD JOURNAL OF GASTROENTEROLOGY
Volume 11, Issue 7, Pages 990-999Publisher
BAISHIDENG PUBLISHING GROUP INC
DOI: 10.3748/wjg.v11.i7.990
Keywords
Acute pancreatitis; Peptide delivery; Penetratin; NF-kappa B inhibition
Categories
Funding
- National Research Foundation (OTKA) [T30735, T042589]
Ask authors/readers for more resources
AIM: To assess the effect of our novel cell-permeable nuclear factor-kappaB (NF-kappa B) inhibitor peptide PN50 in an experimental model of acute pancreatitis. PN50 was produced by conjugating the cell-penetrating penetratin peptide with the nuclear localization signal of the NF-kappa B p50 subunit. METHODS: Pancreatitis was induced in male Wistar rats by administering 2x100 mu g/kg body weight of cholecystokinin-octapeptide (CCK) intraperitoneally (IP) at an interval of 1 h. PN50-treated animals received 1 mg/kg of PN50 IP 30 min before or after the CCK injections. The animals were sacrificed 4 h after the first injection of CCK. RESULTS: All the examined laboratory (the pancreatic weight/body weight ratio, serum amylase activity, pancreatic levels of TNF-alpha and IL-6, degree of lipid peroxidation, reduced glutathione levels, NF-kappa B binding activity, pancreatic and lung myeloperoxidase activity) and morphological parameters of the disease were improved before and after treatment with the PN50 peptide. According to the histological findings, PN50 protected the animals against acute pancreatitis by favoring the induction of apoptotic, as opposed to necrotic acinar cell death associated with severe acute pancreatitis. CONCLUSION: Our study implies that reversible inhibitors of stress-responsive transcription factors like NF-kappa B might be clinically useful for the suppression of the severity of acute pancreatitis. (C) 2005 The WJG Press and Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available