Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/30422
Title: Pregabalin ameliorates lipopolysaccharide-induced pancreatic inflammation in aged rats
Authors: Ozmen, O.
Topsakal, Şenay
Keywords: Immunohistochemistry
Lipopolysaccharide
Pancreas
Pathology
Pregabalin
Rat
amylase
caspase 3
glucose
granulocyte colony stimulating factor
inducible nitric oxide synthase
interleukin 6
lipopolysaccharide
pregabalin
triacylglycerol lipase
antiinflammatory agent
autacoid
Casp3 protein, rat
Il6 protein, rat
Nos2 protein, rat
serum amyloid A
aging
animal experiment
animal model
animal tissue
Article
biochemical analysis
cell infiltration
controlled study
female
histopathology
immune response
immunohistochemistry
leucocyte infiltration
neutrophil chemotaxis
nonhuman
pancreatitis
protein expression
rat
sepsis
single drug dose
animal
blood
cell protection
disease model
drug effect
metabolism
pancreas
pathology
signal transduction
Wistar rat
Animals
Anti-Inflammatory Agents
Caspase 3
Cytoprotection
Disease Models, Animal
Female
Granulocyte Colony-Stimulating Factor
Inflammation Mediators
Interleukin-6
Lipopolysaccharides
Nitric Oxide Synthase Type II
Pancreatitis
Rats, Wistar
Serum Amyloid A Protein
Signal Transduction
Publisher: Bentham Science Publishers
Abstract: 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. © 2019 Bentham Science Publishers.
URI: https://hdl.handle.net/11499/30422
https://doi.org/10.2174/1871530319666190306095532
ISSN: 1871-5303
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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