Abstract
BackgroundAcute respiratory distress syndrome (ARDS) is a complication caused by pulmonary and/or external factors. In this study, we investigated the protective mechanisms of glabridin in lipopolysaccharide (LPS) induced ARDS in rats.ResultsGLA treatment at dose of 30 mg/kg decreased LPS-induced lung W/D ratio and alleviated evident lung histopathological changes. Expressions of TNF-α and IL-18 were suppressed by GLA in plasma. The levels of SPA, MDA and NO in lung were down-regulated significantly in groups administrated with GLA. While the SOD level increased after GLA administration. Additionally, the attenuation of inflammatory responses by GLA was closely associated with p38MAPK/ERK pathway, and the expressions of protein p-p38MAPK and pERK were inhibited by GLA in LPS-induced ARDS rats.Materials and MethodsSixty-four Wistar rats were randomly assigned into control group, Glabridin (GLA) alone group, LPS groups (6 h, 12 h, 24 h), GLA with LPS groups (6 h, 12 h, 24 h). ARDS was induced in rats by intraperitoneal administration of LPS (10 mg/kg). The degree of lung edema was evaluated by calculating the wet/dry weight ratio. The levels of inflammatory mediators, tumor necrosis factor-α (TNF-α) and interleukin-18 (IL-18) were assayed by enzyme-linked immunosorbent assay (ELISA). Surfactant protein A (SPA), malondialdehyde (MDA), nitric oxide (NO) and superoxide dismutase (SOD) were analyzed. Pathological changes of lung tissues were observed by H&E staining. The protein expression of p38MAPK and ERK was detected using immunohistochemical techniques. Lung phosphorylated p38MAPK (p-p38MAPK) and pERK protein expression changes were detected by Western blotting.ConclusionsGlabridin significantly ameliorated the lung injury induced by LPS in rats via the inhibition of p38MAPK and ERK signaling pathway, antioxidant effect and reducing inflammation.
Highlights
The attenuation of inflammatory responses by GLA was closely associated with p38MAPK/ERK pathway, and the expressions of protein p-p38MAPK and pERK were inhibited by GLA in LPSinduced Acute respiratory distress syndrome (ARDS) rats
Glabridin significantly ameliorated the lung injury induced by LPS in rats via the inhibition of p38MAPK and ERK signaling pathway, antioxidant effect and reducing inflammation
Sepsis is a common complication among clinical critical patients, which may lead to multiple organ dysfunction syndrome (MODS)
Summary
Sepsis is a common complication among clinical critical patients, which may lead to multiple organ dysfunction syndrome (MODS). Acute respiratory distress syndrome (ARDS) is a complication that arises in the intensive care unit and contribute to remarkable morbidity and mortality. It is characterized by increased pulmonary alveolar capillary membrane permeability caused by various pathogenic factors. Mitogen activated protein kinases (MAPKs) signaling pathway is the major signal transduction pathways regulating the production of inflammatory cells and has a close relationship with the LPS-induced ARDS [3]. The present study aims to investigate the protective effect and possible mechanism of glabridin on ARDS through LPS-induced ARDS model in rats. Acute respiratory distress syndrome (ARDS) is a complication caused by pulmonary and/or external factors. We investigated the protective mechanisms of glabridin in lipopolysaccharide (LPS) induced ARDS in rats
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