ArticleNaunyn-Schmiedeberg's archives of pharmacology2017
Nilotinib, a tyrosine kinase inhibitor exhibits protection against acute pancreatitis-induced lung and liver damage in rats.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Pancreatic Elastase Affects Liver Injury by Activating Proinflammatory Cytokines in Kupffer Cells via the JAK2/STAT3 Signaling Pathway.Current molecular medicine · 2026Article
- Duloxetine ameliorates acute pancreatitis-associated inflammation and modulates pain related neuroinflammatory pathways via modulation of SP-related neurokinin signaling and PAR2/TRPV1 pathways.Frontiers in toxicology · 2026Article
- Liver injury associated with acute pancreatitis: The current status of clinical evaluation and involved mechanisms.World journal of clinical cases · 2021Review
- Examining the Early Period Effect of Nilotinib on Hearing: An Experimental Study.The journal of international advanced otology · 2020Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This investigation explored the nilotinib action in the management of acute pancreatitis (AP) and AP-induced lung and liver injury. AP was induced in Sprague Dawley (SD) rats with L-arginine. Treatment with nilotinib with or without L-arginine was applied for 7 days. Marked deterioration in serum amylase, lipase, aspartate amino transferase (AST), alanine amino transferase (ALT), lactate dehydrogenase (LDH), nitric oxide (NO), total protein content, and transforming growth factor beta1 (TGF-β1) along with pancreatic, hepatic, and pulmonary tissue lipid peroxidation (MDA) after induction of AP while significant reduction in tissues superoxide dismutase (SOD), glutathione (GSH) with marked edema, hemorrhage, and perivascular inflammation with acinar cell necrosis, along with elevated pancreatic percentage expression of TGF-β1 and nuclear factor kappa B (NF-κB), were observed in the AP group. Nilotinib markedly ameliorated biochemical and histopathologic changes during AP, thus preserving the pancreas, liver, and lung histologically through mechanism involving antioxidant and anti-inflammatory actions.
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Registered trials
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