title: Protective effect of β-glucan on acute lung injury induced by lipopolysaccharide in rats.
abstract: OBJECTIVE
  Lipopolysaccharide (LPS)-induced endotoxemia can cause serious organ damage such as acute lung injury and death by triggering the secretion of proinflammatory cytokines and acute-phase reactants. The goal of this study was to evaluate the effects of β-glucan on inflammatory mediator levels and histopathological changes in LPS-induced endotoxemia.
  
  
  METHODS
  Forty-seven male Wistar albino rats were randomly allocated into four groups as follows: control group, LPS group (10 mg/kg LPS), LPS + β-glucan group (100 mg/kg β-glucan before LPS administration), and β-glucan group. Twelve hours after LPS administration, lung and serum samples were collected. Concentrations of IL-6, IL-8, C-reactive protein (CRP), and procalcitonin were measured in the serum at hours 0 (basal) and 12. The severity of lung damage was assessed by an appropriate histopathological scoring system.
  
  
  RESULTS
  Serum levels of CRP in the LPS group at 12 h were significantly higher than in the other groups, whereas serum IL-6 levels in the LPS and LPS + β-glucan groups at 12 h were significantly decreased. The mean histopathological damage score of the LPS group was slightly higher than that of the LPS + β-glucan group. Moreover, mortality rate was significantly decreased in the LPS + β-glucan group versus the LPS group.
  
  
  CONCLUSIONS
  β-glucan reduces endotoxemia-induced mortality and might be protective against endotoxemia-induced lung damage.
authors.forename: Meryem
authors.initials: M
authors.lastname: Iraz
authors.forename: Mustafa
authors.initials: M
authors.lastname: Iraz
authors.forename: Mukaddes
authors.initials: M
authors.lastname: Eşrefoğlu
authors.forename: Mehmet Şerif
authors.initials: MŞ
authors.lastname: Aydin
mesh_terms: D055371:Acute Lung Injury / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D000209:Acute-Phase Proteins / Q000378:metabolism; D000818:Animals; D001685:Biological Factors / Q000494:pharmacology; D002097:C-Reactive Protein / Q000378:metabolism; D019446:Endotoxemia / Q000139:chemically induced / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008168:Lung / Q000473:pathology; D008297:Male; D020011:Protective Agents / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D047071:beta-Glucans / Q000494:pharmacology*
chemical_list: D000209:Acute-Phase Proteins; D001685:Biological Factors; D015850:Interleukin-6; D016209:Interleukin-8; D008070:Lipopolysaccharides; D020011:Protective Agents; D047071:beta-Glucans; D002097:C-Reactive Protein