ArticleWorld journal of gastroenterology2005
A nuclear import inhibitory peptide ameliorates the severity of cholecystokinin-induced acute pancreatitis.
Article in World journal of gastroenterology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 39 citations in OpenAlex.
- Potential of oligonucleotide- and protein/peptide-based therapeutics in the management of toxicant/stressor-induced diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Stereoisomer-Dependent Membrane Association and Capacity for Insulin Delivery Facilitated by Penetratin.Pharmaceutics · 2023Article
- Ferulic acid attenuates pancreaticobiliary duct occlusion-induced inflammation in both pancreas and liver.Inflammopharmacology · 2023Article
- Azithromycin Polarizes Macrophages to an M2 Phenotype via Inhibition of the STAT1 and NF-κB Signaling Pathways.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- LincRNA-Gm4419 knockdown ameliorates NF-κB/NLRP3 inflammasome-mediated inflammation in diabetic nephropathy.Cell death & disease · 2017Article
- Inhibition of pancreatic oxidative damage by stilbene derivative dihydro-resveratrol: implication for treatment of acute pancreatitis.Scientific reports · 2016Article
- Article
- Essential role of monocytes and macrophages in the progression of acute pancreatitis.World journal of gastroenterology · 2010Review
- Therapeutic proteasome inhibition in experimental acute pancreatitis.World journal of gastroenterology · 2007Article
- Inhibitors of NF-kappaB signaling: 785 and counting.Oncogene · 2006Review
- Inhibiting NF-κB activation by small molecules as a therapeutic strategy.Biochimica et biophysica actaReview
- NF-κB as a Therapeutic Target in Inflammatory-Associated Bone Diseases.Advances in protein chemistry and structural biologyReview
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo assess the effect of our novel cell-permeable nuclear factor-kappaB (NF-kappaB) 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-kappaB p50 subunit.
methodsPancreatitis was induced in male Wistar rats by administering 2X100 mug/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.
resultsAll 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-kappaB 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.
conclusionOur study implies that reversible inhibitors of stress-responsive transcription factors like NF-kappaB might be clinically useful for the suppression of the severity of acute pancreatitis.
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