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Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
Dendrobine attenuates lipopolysaccharide-induced acute lung injury by modulating FAM134B-mediated endoplasmic
Jia Zhou1, Sanzhong Li2, Zhiguo Hu3
1Department of Critical Care Medicine, Medical Center of Anesthesiologyand Pain, The First Affliated Hospital, Jiangxi Medical College, NanchangUniversity, Nanchang 330006, PR China; Jiangxi Institute of Respiratory Disease, Nanchang 330052, PR China.
Background:
Macrophage-mediated excessive inflammatory responses play a pivotal role in sepsis progression, particularly in the lungs. Endoplasmic reticulum stress (ERS) and mitochondrial dysfunction, also contribute to the development of acute lung injury (ALI). Dendrobine is a natural alkaloid known to alleviate ERS in various diseases; however, its specific role in sepsis-associated ALI is not yet fully understood.
Objective:
This study investigates the protective effects of dendrobine against ALI and elucidates the underlying mechanisms.
Methods:
We assessed the protective effects of dendrobine using LPS-induced THP-1 cells and a murine model of sepsis. Techniques included HE staining for lung tissue damage, TUNEL staining for pulmonary apoptosis, flow cytometry for intracellular reactive oxygen species (ROS) levels and apoptosis, transmission electron microscopy for ER autophagy and changes in mitochondria-associated ER membranes (MAMs), and confocal microscopy for ER autophagy flux, mitochondrial membrane potential, and mitochondrial calcium ion levels.
Results:
Dendrobine significantly alleviated LPS-induced ALI and inflammatory responses in mice by reducing the expression of ERS-related and pro-apoptotic proteins. It enhanced ER autophagy by upregulating FAM134B, inhibiting its ubiquitination and degradation, and promoting its interaction with LC3B. Dendrobine partially restored LPS-induced mitochondrial dysfunction by reducing MAM formation. Conversely, FAM134B knockdown reversed the protective effects of dendrobine.
Conclusion:
This study demonstrates that dendrobine alleviates LPS-induced ERS and mitochondrial dysfunction through FAM134B-mediated ER autophagy and MAM reduction, thereby protecting lung tissue. These findings highlight the potential of dendrobine as a therapeutic agent against sepsis-induced ALI.
Insights
Dendrobine protects against sepsis-induced acute lung injury (ALI) by reducing endoplasmic reticulum stress (ERS) and mitochondrial dysfunction. This natural compound enhances ER autophagy via FAM134B, offering potential therapeutic benefits for ALI.
Area of Science:
- Cellular Biology
- Immunology
- Pharmacology
Background:
- Sepsis-induced acute lung injury (ALI) involves excessive inflammation, endoplasmic reticulum stress (ERS), and mitochondrial dysfunction.
- Dendrobine, a natural alkaloid, is known to alleviate ERS but its role in sepsis-associated ALI requires investigation.
Purpose of the Study:
- To investigate the protective effects of dendrobine against ALI in a sepsis model.
- To elucidate the underlying mechanisms of dendrobine's action, focusing on ERS and mitochondrial pathways.
Main Methods:
- Utilized LPS-induced THP-1 cells and a murine sepsis model.
- Assessed lung tissue damage, apoptosis, reactive oxygen species (ROS), ER autophagy, mitochondrial function, and MAMs.
Main Results:
- Dendrobine significantly reduced ALI and inflammation in mice by decreasing ERS and pro-apoptotic proteins.
- Enhanced ER autophagy through FAM134B upregulation and promoted its interaction with LC3B.
- Partially restored mitochondrial function by reducing MAM formation; FAM134B knockdown reversed these effects.
Conclusions:
- Dendrobine alleviates LPS-induced ERS and mitochondrial dysfunction via FAM134B-mediated ER autophagy and MAM reduction.
- Dendrobine demonstrates potential as a therapeutic agent for sepsis-induced ALI.
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