Abstract:

Aim/Background: Currently, acute pancreatitis pathogenesis remains a matter of debate. Our study aims to investigate the oxidative stress and lipid peroxidation state in taurocholate-induced acute pancreatitis, and we used oxidized LDL as a biomarker of oxidative stress. Methods: We used twenty-six Wistar albino rats divided into four groups. Sham-operated rats, control group (group 1), and experimental group with sodium taurocholate-induced acute pancreatitis; were sacrificed at 24 hours (group 2), 48 hours (group 3), and 72 hours (group 4). We evaluated pancreatic tissue malondialdehyde (MDA) levels as an indicator of lipid peroxidation. Then, using the immunofluorescence staining, we determined the presence of ox-LDL in pancreatic tissues, which we used to compare the histopathological analysis of pancreatitis. Results: We found that MDA levels in pancreatic tissue and serum amylase, ALT, and AST were significantly higher in groups 2, 3, and 4. Histopathological findings of groups 2, 3, and 4 were compatible with pancreatitis, and we encountered the level of ox-LDL accumulation. We found a parallelism between the level of ox-LDL accumulation in pancreatic tissue and the severity of pancreatitis in groups 2, 3, and 4. Conclusion: This study demonstrates the accumulation of ox-LDL molecules in pancreatic tissue in a taurocholate-induced acute pancreatitis model. According to these byproducts, including ox-LDL, we conceive that treatment modalities might have beneficial effects in improving not local but systemic complications of acute pancreatitis.

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