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Updated: Sep 19, 2026
Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
Attenuation of Neutrophil Extracellular Trap Formation in Lipopolysaccharide-Induced Acute Lung Injury Associated
Nian Cao1, Yue Dai1, Juan Feng1
1Department of Pulmonary and Critical Care Medicine, The Third Clinical Medical College of the Three Gorges University, Gezhouba Central Hospital of Sinopharm, Yichang, Hubei Province, China.
Background:
Excessive neutrophil activation and neutrophil extracellular trap (NET) formation play critical roles in the pathogenesis of acute lung injury (ALI). Cinnamaldehyde, a major bioactive component of cinnamon, has been reported to exert anti-inflammatory effects; however, its impact on NET formation in ALI remains unclear.
Methods:
A lipopolysaccharide (LPS)-induced ALI rat model and a PMA-stimulated primary neutrophil model were employed to evaluate the effects of cinnamaldehyde in vivo and in vitro. Lung injury severity, pulmonary edema, inflammatory cell infiltration, cytokine production, and NET-associated markers were assessed using histopathology, wet-to-dry ratio analysis, BALF examination, immunofluorescence staining, and Western blotting.
Results:
Cinnamaldehyde significantly alleviated LPS-induced lung injury, as evidenced by reduced lung wet-to-dry ratios and improved histopathological scores compared with the LPS group (p < .001). Treatment with cinnamaldehyde markedly decreased inflammatory cell and neutrophil infiltration in BALF and suppressed TNF-α, IL-6, and MCP-1 levels (p < .05-0.001). Furthermore, cinnamaldehyde significantly inhibited NET formation in lung tissues, as indicated by reduced levels of myeloperoxidase, cell-free DNA, citrullinated histone H3, and neutrophil elastase (p < .001). In vitro, cinnamaldehyde directly suppressed PMA-induced NET release from primary neutrophils without affecting cell viability (p < .001).
Conclusion:
These findings demonstrate that cinnamaldehyde protects against LPS-induced acute lung injury by suppressing excessive NET formation, highlighting NET inhibition as a key mechanism underlying its pulmonary protective effects.
