AI Article Synopsis
- The study investigated how nilotinib affects acute pancreatitis (AP) and its impact on lung and liver injury in rats.
- Induction of AP led to significant decreases in several key biochemical markers and increased tissue damage, including inflammation and cell death in pancreatic tissues.
- Treatment with nilotinib notably improved these conditions, showing its potential as an antioxidant and anti-inflammatory agent that can protect tissues from damage during AP.
Article 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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