Objective: The aim of this study was to examine pancreatic pathology and the prophylactic
effects of pregabalin in lipopolysaccharide (LPS) induced sepsis model in aged rats.
Methods: Twenty-four female, one-year-old, Wistar Albino rats were assigned to three groups; Group I
(control), Group II (study group: 5mg/kg LPS intraperitoneal, single dose) and Group III(treatment
group: 5mg/kg LPS+30 mg/kg oral pregabalin one hour before LPS). Animals were sacrificed by exsanguination
6 hours after LPS administration. Blood and pancreatic tissue samples were collected for
biochemical, pathological, and immunohistochemical analyses.
Results: LPS caused increases in serum amylase and lipase level but led to a reduction in glucose levels.
Following histopathological analysis, numerous neutrophil leucocyte infiltrations were observed in vessels
and pancreatic tissues. Increased caspase-3 expression was observed in both the endocrine and exocrine
pancreas in the LPS group. Similarly, IL-6, caspase-3 (Cas-3), inducible nitric oxide synthase
(iNOS), granulocyte colony-stimulating factor (G-CSF) and serum amyloid-A (SAA) expressions were
increased by LPS. Pregabalin improved biochemical, histopathological, and immunohistochemical findings.
Conclusion: This study showed that LPS causes pathological findings in the pancreas, but pregabalin
has ameliorative effects in aged rats with sepsis. Cas-3, IL-6, iNOS, G-CSF, and SAA all play pivotal
roles in the pathogenesis of LPS-induced pancreatic damage.