title: S-Nitrosoglutathione ameliorates acute renal dysfunction in a rat model of lipopolysaccharide-induced sepsis.
abstract: OBJECTIVE
  Sepsis induces an inflammatory response that results in acute renal failure (ARF). The current study is to evaluate the role of S-Nitrosoglutathione (GSNO) in renoprotection from lipopolysaccharide (LPS)-induced sepsis.
  
  
  METHODS
  Rats were divided to three groups. First group received LPS (5 mg/kg body weight), second group was treated with LPS + GSNO (50 μg/kg body weight), and third group was administered with vehicle (saline). They were sacrificed on day 1 and 3 post-LPS injection. Serum levels of nitric oxide (NO), creatinine and blood urea nitrogen (BUN) were analysed. Tissue morphology, T lymphocyte infiltrations, and the expression of inflammatory (TNF-α, iNOS) and anti-inflammatory (IL-10) mediators as well as glutathione (GSH) levels were determined.
  
  
  RESULTS
  Lipopolysaccharide significantly decreased body weight and increased cellular T lymphocyte infiltration, caspase-3 and iNOS and decreased PPAR-γ in renal tissue. NO, creatinine and BUN were significantly elevated after LPS challenge, and they significantly decreased after GSNO treatment. TNF-α level was found significantly increased in LPS-treated serum and kidney. GSNO treatment of LPS-challenged rats decreased caspase-3, iNOS, TNF-α, T lymphocyte infiltration and remarkably increased levels of IL-10, PPAR-γ and GSH.
  
  
  CONCLUSIONS
  GSNO can be used as a renoprotective agent for the treatment of sepsis-induced acute kidney injury.
authors.affiliation: Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, SC, USA.
authors.forename: Devadoss J
authors.initials: DJ
authors.lastname: Samuvel
authors.affiliation: Department of Pediatrics, Medical University of South Carolina, Charleston, SC, USA.
authors.forename: Anandakumar
authors.initials: A
authors.lastname: Shunmugavel
authors.affiliation: Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, SC, USA.
authors.forename: Avtar K
authors.initials: AK
authors.lastname: Singh
authors.affiliation: Department of Pediatrics, Medical University of South Carolina, Charleston, SC, USA.
authors.forename: Inderjit
authors.initials: I
authors.lastname: Singh
authors.affiliation: Department of Pediatrics, Medical University of South Carolina, Charleston, SC, USA. khanm@musc.edu.
authors.forename: Mushfiquddin
authors.initials: M
authors.lastname: Khan
mesh_terms: D058186:Acute Kidney Injury / Q000097:blood / Q000139:chemically induced / Q000188:drug therapy*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001806:Blood Urea Nitrogen; D053148:Caspase 3 / Q000378:metabolism; D003404:Creatinine / Q000097:blood; D005260:Female; D005978:Glutathione / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D026422:S-Nitrosoglutathione / Q000494:pharmacology*; D018805:Sepsis / Q000097:blood / Q000139:chemically induced* / Q000188:drug therapy* / Q000378:metabolism; D013601:T-Lymphocytes / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D009569:Nitric Oxide; D026422:S-Nitrosoglutathione; D003404:Creatinine; D052247:Nitric Oxide Synthase Type II; D053148:Caspase 3; D005978:Glutathione
keywords: S-Nitrosoglutathione; acute kidney injury; lipopolysaccharide; renoprotection; sepsis