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Updated: Jun 4, 2026
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Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
Ascorbic acid attenuates lipopolysaccharide-induced acute lung injury
Bernard J Fisher1, Ignacio M Seropian, Donatas Kraskauskas
1Division of Pulmonary Disease and Critical Care Medicine, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Critical Care Medicine
|March 2, 2011
Summary
Parenteral ascorbic acid treatment improved survival and lung function in a mouse model of sepsis-induced acute lung injury. This intervention reduced inflammation and blood clotting, offering a potential therapeutic avenue for sepsis complications.
Area of Science:
- Pulmonary Medicine
- Critical Care Medicine
- Biochemistry
Background:
- Sepsis-induced lung injury is a significant clinical challenge lacking direct therapeutic options.
- Intravenous ascorbic acid has shown promise in improving sepsis-related circulatory dysfunction.
- The pro-inflammatory and pro-coagulant state in sepsis contributes to lung injury.
Purpose of the Study:
- To investigate whether parenteral ascorbic acid administration can modulate the inflammatory and clotting responses in endotoxin-induced acute lung injury.
- To determine the therapeutic potential of ascorbic acid in a preclinical model of sepsis-induced lung vascular injury.
Main Methods:
- C57BL/6 mice were administered lethal doses of lipopolysaccharide to induce acute lung injury.
- Ascorbic acid or dehydroascorbic acid was administered intraperitoneally 30 minutes post-lipopolysaccharide exposure.
- Key outcomes measured included survival, lung capillary leak, inflammatory chemokine expression, and microvascular thrombosis.
Main Results:
- Lipopolysaccharide induced 100% mortality within 28 hours, characterized by severe lung inflammation and thrombosis.
- Treatment with ascorbic acid or dehydroascorbic acid significantly prolonged survival and preserved lung architecture.
- Both forms of vitamin C attenuated inflammation, reduced capillary leak, inhibited microvascular thrombosis, and normalized coagulation parameters.
Conclusions:
- Interventional administration of ascorbic acid following lipopolysaccharide exposure effectively mitigates the pro-inflammatory and pro-coagulant state driving lung vascular injury.
- Ascorbic acid demonstrates therapeutic potential in an animal model of sepsis-induced acute lung injury, highlighting its role in managing sepsis complications.
