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Updated: Apr 15, 2026
Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
Fucosterol attenuates lipopolysaccharide-induced acute lung injury in mice
Yuexia Li1, Xiaohui Li2, Gang Liu1
1Intensive Care Unit, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.
Background:
Fucosterol has been reported to have antioxidant, antidiabetic, and anti-inflammatory effects. In this study, we investigated the protective effect and the possible mechanism of fucosterol on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice.
Methods:
Lung injury was assessed by a histologic study, pulmonary edema, and inflammatory cytokines production in bronchoalveolar lavage fluid. Alveolar macrophages were stimulated with LPS in the presence or absence of fucosterol. The expressions of inflammatory cytokines were determined by enzyme-linked immunosorbant assay. Nuclear factor-kappa B (NF-κB) expression was detected by Western blotting.
Results:
The results showed that fucosterol attenuated lung histopathologic changes, wet-to-dry ratio, and tumor necrosis factor-α, interleukin (IL)-6 and IL-1β production in LPS-induced ALI in mice. Meanwhile, fucosterol inhibited NF-κB activation and tumor necrosis factor-α, IL-6, and IL-1β production in LPS-stimulated alveolar macrophages.
Conclusions:
In conclusion, the present study demonstrated that fucosterol exhibited a protective effect on LPS-induced acute lung injury, and the possible mechanism is involved in inhibiting NF-κB activation, thereby inhibiting LPS-induced inflammatory response.
