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Updated: May 14, 2026
Halogenated Agent Delivery in Porcine Model of Acute Respiratory Distress Syndrome via an Intensive Care Unit Type Device
Published on: September 24, 2020
Hydrogen sulfide donor regulates alveolar epithelial cell apoptosis in rats with acute lung injury
Wen-li Liu1, Zhi-wei Liu, Tian-shui Li
1Department of Emergency Medicine, Beijing Jishuitan Hospital, Beijing 100035, China.
Background:
Acute lung injury (ALI) is a common syndrome associated with high morbidity and mortality in emergency medicine. Cell apoptosis plays a key role in the pathogenesis of ALI. Hydrogen sulfide (H(2)S) plays a protective role during acute lung injury. We designed this study to examine the role of H(2)S in the lung alveolar epithelial cell apoptosis in rats with ALI.
Methods:
Sixty-nine male Sprague Dawley rats were used. ALI was induced by intra-tail vein injection of oleic acid (OA). NaHS solution was injected intraperitonally 30 minutes before OA injection as the NaHS pretreatment group. Single sodium hydrosulfide pretreatment group and control group were designed. Index of quantitative assessment (IQA), wet/dry weight (W/D) ratio and the percentage of polymorphonuclear leukocyte (PMN) cells in the bronchoalveolar lavage fluid (BALF) were determined. H(2)S level in lung tissue was measured by a sensitive sulphur electrode. Apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and Fas protein was measured by immunohistochemical staining.
Results:
The level of endogenous H(2)S in lung tissue decreased with the development of ALI induced by OA injection. Apoptosis and Fas protein in alveolar epithelial cells increased in the ALI of rats but NaHS lessened apoptosis and Fas protein expression in alveolar epithelial cells of rats with ALI.
Conclusion:
Endogenous H(2)S protects rats from oleic acid-induced ALI, probably by inhibiting cell apoptosis.
