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Untargeted lipidomics of bronchopulmonary dysplasia induced by hyperoxia exposure in rats
Yubai Li1, Qian Su1, Xudong Yan1
1Division of Neonatology, Department of Pediatrics, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.
Insights
This study reveals significant alterations in lung lipid profiles in a rat model of bronchopulmonary dysplasia (BPD). Key lipids like triacylglycerol and phosphatidylcholine were notably decreased, offering potential therapeutic targets for BPD.
Area of Science:
- Neonatal physiology
- Pulmonary medicine
- Lipidomics
Background:
- Bronchopulmonary dysplasia (BPD) is a major cause of death in premature infants, linked to abnormal lung development.
- Lipid synthesis and metabolism are crucial for lung development and pulmonary surfactant (PS) production.
- Understanding lipid changes in BPD is vital for identifying therapeutic strategies.
Purpose of the Study:
- To investigate pulmonary lipid composition changes during BPD progression using a rat model.
- To identify specific lipids affected by hyperoxia-induced lung injury.
Main Methods:
- Neonatal Sprague-Dawley rats were exposed to hyperoxia for 14 days.
- Lung tissues underwent pathological analysis (H&E staining).
- Untargeted lipidomics was performed using liquid chromatography-tandem mass spectrometry (LC-MS/MS).
Main Results:
- Hyperoxia exposure led to enlarged alveoli, reduced alveolar count, and decreased surfactant protein D (SFTPD).
- LC-MS/MS identified 620 pulmonary lipids across 27 categories, with triacylglycerol (TAG), phosphatidylcholine (PC), and phosphatidylethanolamine (PE) being most abundant.
- Overall lung lipid levels decreased in hyperoxia-exposed rats, with significant reductions in TAG and PC.
Conclusions:
- Hyperoxia significantly alters lung lipid profiles in neonatal rats, mimicking aspects of BPD.
- Decreased levels of TAG and PC suggest their involvement in BPD pathogenesis.
- These findings provide insights for identifying potential therapeutic targets and biomarkers for BPD.
Background:
Bronchopulmonary dysplasia (BPD), characterized by impaired lung development, remains a leading cause of morbidity and mortality in premature infants. The synthesis and metabolism of lipids play a critical role in normal lung development, such as dipalmitoylphosphatidylcholine, a key component of pulmonary surfactant (PS). Therefore, we conducted a lipidomics study of rat lung tissue to explore the changes of pulmonary lipid composition in the progression of BPD disease.
Methods:
In this study, we exposed neonatal Sprague-Dawley (SD) rats to hyperoxia for 14 days. After hyperoxia exposure, the lung tissues of rats were analyzed pathologically, and untargeted lipidomics was analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS).
Results:
Hematoxylin-eosin (H&E) staining showed that the alveoli enlarged, the number of alveoli decreased and the pulmonary surfactant-associated protein D (SFTPD) decreased in hyperoxia-exposed rats. A total of 620 pulmonary lipids were detected by LC-MS/MS, covering 27 lipid categories. The most common lipids were triacylglycerol (TAG), followed by phosphatidylcholine (PC) and phosphatidylethanolamine (PE).
Conclusions:
Compared with those rats exposed to normoxic conditions, the lipid levels in the lungs of rats exposed to hyperoxia for 14 days generally decreased, with the levels of TAG and PC decreasing most significantly. In short, our results provide a clue for finding therapeutic targets and biomarkers of a BPD rat model lung liposome.
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