4.5 Article

Glycyrrhizin Treatment Is Associated with Attenuation of Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting Cyclooxygenase-2 and Inducible Nitric Oxide Synthase Expression

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JOURNAL OF SURGICAL RESEARCH
卷 165, 期 1, 页码 E29-E35

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ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.jss.2010.10.004

关键词

glycyrrhizin; lipopolysaccharide; acute lung injury; cyclooxygenase-2; Inducible nitric oxide synthase

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资金

  1. Military Medical Scientific Research Items of China [06MA206]

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Glycyrrhizin (GL), a major active constituent of licorice root, has been attributed numerous pharmacologic effects, including anti-inflammatory, anti-viral, anti-tumor, and hepatoprotective activities. In this study, we investigated the anti-inflammatory effect of GL on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. ALI was induced in Balb/c mice by intratracheal instillation of LPS (1 mg/kg). Before 1 h of LPS administration, the mice received intraperitoneal injection of GL at varied doses (10, 25, and 50 mg/kg). The severity of pulmonary injury was evaluated 12 h after LPS administration. GL pretreatment led to significant attenuation of LPS induced evident lung histopathologic changes, alveolar hemorrhage, and neutrophil infiltration with evidence of reduced myeloperoxidase (MPO) activity. The lung wet/dry weight ratios, as an index of lung edema, were markedly reduced by GL pretreatment. The concentrations of pro-inflammatory cytokines interleukin (IL)-1 beta and tumor necrosis factor (TNF)-alpha were elevated in bronchoalveolar lavage fluid (BALF) after LPS administration, which were significantly inhibited by GL pretreatment. GL pretreatment also reduced the concentrations of nitric oxide (NO) in lung tissues. Furthermore, the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) was suppressed by GL pretreatment. In conclusion, GL potently protected against LPS-induced ALI, and the protective effects of GL may attribute partly to the suppression of COX-2 and iNOS expression. (C) 2011 Elsevier Inc. All rights reserved.

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