Turkish Journal of Medical Sciences




Background/aim: 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 \beta-glucan on inflammatory mediator levels and histopathological changes in LPS-induced endotoxemia. Materials and methods: Forty-seven male Wistar albino rats were randomly allocated into four groups as follows: control group, LPS group (10 mg/kg LPS), LPS + \beta-glucan group (100 mg/kg \beta-glucan before LPS administration), and \beta-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 + \beta-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 + \beta-glucan group. Moreover, mortality rate was significantly decreased in the LPS + \beta-glucan group versus the LPS group.


Endotoxin, acute lung injury, \beta-glucan, C-reactive protein, interleukin-6

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