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Alda-1 Protects Against Acrolein-Induced Acute Lung Injury and Endothelial Barrier Dysfunction
Qing Lu1, Miles Mundy1, Eboni Chambers1
1Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, Rhode Island.
American Journal of Respiratory Cell and Molecular Biology
|August 2, 2017
Summary
Acrolein inhalation causes lung edema and injury. Alda-1, an activator of mitochondrial aldehyde dehydrogenase 2, prevented and rescued acrolein-induced lung injury, suggesting a potential treatment for smoke inhalation.
Area of Science:
- Toxicology
- Pulmonary Medicine
- Biochemistry
Background:
- Acrolein inhalation is a significant cause of lung edema and acute lung injury.
- The precise mechanisms underlying acrolein toxicity and effective treatments remain poorly understood.
Purpose of the Study:
- To elucidate the mechanisms of acrolein-induced lung injury.
- To investigate the therapeutic potential of Alda-1 and AMP-activated protein kinase (AMPK) activation.
Main Methods:
- Dose-dependent induction of lung edema and LPS-induced acute lung injury in animal models.
- Assessment of endothelial cell permeability, adherens junctions, and focal adhesion complexes in primary cultured lung microvascular endothelial cells (LMVECs).
- Evaluation of mitochondrial function, reactive oxygen species (ROS) production, and AMPK signaling pathways.
Main Results:
- Acrolein dose-dependently induced lung edema and exacerbated LPS-induced acute lung injury.
- Alda-1 effectively prevented and rescued acrolein-induced lung injury and endothelial barrier dysfunction.
- Acrolein disrupted endothelial cell junctions and inhibited AMPK signaling, while Alda-1 and N-acetylcysteine attenuated these effects.
Conclusions:
- Acrolein-induced mitochondrial dysfunction may not directly cause endothelial barrier dysfunction.
- Alda-1 and AMPK activation represent promising therapeutic strategies for acrolein-associated acute lung injury, particularly following smoke inhalation.
