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Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
Punicalagin ameliorates lipopolysaccharide-induced acute respiratory distress syndrome in mice
Jingjing Peng1, Dong Wei, Zengqiang Fu
1Department of Oncology, The General Hospital of Chengdu Military District, Chengdu, Sichuan, 610000, People's Republic of China.
Abstract:
Punicalagin, a bioactive ellagitannin isolated from pomegranate, has been reported to have anti-inflammatory property. In the present study, we analyzed the role of punicalagin against acute respiratory distress syndrome (ARDS) induced by lipopolysaccharide (LPS) in mice. Male BALB/c mice with ARDS, induced by intranasal instillation of LPS, were treated with punicalagin 1 h prior to LPS exposure. The effects of punicalagin on pro-inflammatory cytokines, myeloperoxidase activity, nuclear factor kappa B (NF-κB) activation, and the histopathological changes were evaluated. The results showed that punicalagin treatment attenuated LPS-induced lung edema, elevating TNF-α, IL-6, and IL-1β levels in the bronchoalveolar lavage fluid (BALF). Meanwhile, punicalagin significantly inhibited LPS-induced increases in the macrophage and neutrophil infiltration of lung tissues and myeloperoxidase activity. Furthermore, punicalagin inhibits Toll-like receptor 4 (TLR4) expression and NF-κB activation induced by LPS. In conclusion, this is the first study to demonstrate that punicalagin protects against LPS-induced ARDS in mice. The underlying mechanisms may include inhibition of TLR4-mediated NF-κB signaling pathways.
Insights
Punicalagin, a pomegranate extract, effectively combats acute respiratory distress syndrome (ARDS) in mice. It works by reducing inflammation and inhibiting key signaling pathways involved in ARDS development.
Area of Science:
- Pharmacology
- Immunology
- Toxicology
Background:
- Punicalagin, an ellagitannin from pomegranates, exhibits anti-inflammatory properties.
- Acute Respiratory Distress Syndrome (ARDS) is a severe lung condition often triggered by lipopolysaccharide (LPS).
Purpose of the Study:
- To investigate the protective effects of punicalagin against LPS-induced ARDS in a mouse model.
- To elucidate the underlying molecular mechanisms of punicalagin's action in ARDS.
Main Methods:
- ARDS was induced in BALB/c mice via intranasal LPS instillation.
- Mice were pre-treated with punicalagin before LPS exposure.
- Evaluated lung edema, pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), myeloperoxidase activity, immune cell infiltration, NF-κB activation, and TLR4 expression.
Main Results:
- Punicalagin treatment significantly reduced LPS-induced lung edema and pro-inflammatory cytokine levels in bronchoalveolar lavage fluid.
- It inhibited neutrophil and macrophage infiltration in lung tissues and decreased myeloperoxidase activity.
- Punicalagin suppressed LPS-induced Toll-like receptor 4 (TLR4) expression and NF-κB activation.
Conclusions:
- This study demonstrates punicalagin's protective effect against LPS-induced ARDS in mice.
- The findings suggest punicalagin acts by inhibiting the TLR4-mediated NF-κB signaling pathway.
