Glabridin attenuates lipopolysaccharide-induced acute lung injury by inhibiting p38MAPK/ERK signaling pathway
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Updated: Mar 9, 2026
Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
Li-Peng Zhang1, Yan Zhao2, Guo-Juan Liu1
1Department of Critical Care Medicine, The Affiliated Hospital of Innner Mongolia Medical University, Hohhot 010050, China.
Background:
Acute 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.
Results:
GLA 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 Methods:
Sixty-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.
Conclusions:
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.
Insights
Glabridin (GLA) protects against acute respiratory distress syndrome (ARDS) in rats by reducing lung inflammation and oxidative stress. This protective effect is linked to the inhibition of p38MAPK and ERK signaling pathways.
Area of Science:
- Pharmacology
- Toxicology
- Respiratory Medicine
Background:
- Acute respiratory distress syndrome (ARDS) is a severe lung condition with high mortality.
- Pulmonary and external factors can trigger ARDS.
- Investigating protective mechanisms against ARDS is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the protective effects of glabridin (GLA) in a rat model of lipopolysaccharide (LPS)-induced ARDS.
- To elucidate the underlying mechanisms of GLA's action in mitigating lung injury.
Main Methods:
- Sixty-four Wistar rats were used, divided into control, GLA alone, LPS-induced ARDS, and GLA + LPS groups.
- ARDS was induced via intraperitoneal LPS administration.
- Lung injury was assessed by wet/dry weight ratio, histopathology, inflammatory mediators (TNF-α, IL-18), oxidative stress markers (SPA, MDA, NO, SOD), and p38MAPK/ERK pathway activation (Western blotting, immunohistochemistry).
Main Results:
- GLA treatment (30 mg/kg) reduced lung wet/dry ratio and histopathological damage in LPS-induced ARDS rats.
- GLA suppressed plasma levels of TNF-α and IL-18, and lung levels of MDA and NO, while increasing SOD.
- GLA inhibited the activation of the p38MAPK/ERK signaling pathway, indicated by reduced p-p38MAPK and pERK expression.
Conclusions:
- Glabridin demonstrates significant protective effects against LPS-induced lung injury in a rat model.
- GLA ameliorates ARDS by reducing inflammation and oxidative stress.
- The protective mechanisms involve the inhibition of the p38MAPK and ERK signaling pathways.
