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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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