Hydrogen sulfide donor regulates alveolar epithelial cell apoptosis in rats with acute lung injury

• Published in: Chinese medical journal 2013-02, Vol.126 (3), p.494-499
• Main Authors: Liu, Wen-li, Liu, Zhi-wei, Li, Tian-shui, Wang, Cong, Zhao, Bin
• Format: Article
• Language: English
• Subjects: Acute Lung Injury - chemically induced; Acute Lung Injury - drug therapy; Acute Lung Injury - metabolism; Animals; Apoptosis - physiology; Epithelial Cells - drug effects; Hydrogen Sulfide - metabolism; In Situ Nick-End Labeling; Male; Oleic Acid - toxicity; Rats; Rats, Sprague-Dawley; SD大鼠; Sulfides - pharmacology; Sulfides - therapeutic use; 供体; 免疫组化染色; 急性肺损伤; 支气管肺泡灌洗液; 硫化氢; 细胞凋亡; 肺泡上皮
• ISSN: 0366-6999; 2542-5641
• DOI: 10.3760/cma.j.issn.0366-6999.20120809

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 ALl. Hydrogen sulfide （H2S） plays a protective role during acute lung injury. We designed this study to examine the role of H2S in the lung alveolar epithelial cell apoptosis in rats with ALl. Methods Sixty-nine male Sprague Dawley rats were used. ALI was induced by intra-tail vein injection of oleic acid （OA）. NariS solution was injected intraperitonally 30 minutes before OA injection as the NariS 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. H2S 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 H2S in lung tissue decreased with the development of ALl induced by OA injection. Apoptosis and Fas protein in alveolar epithelial cells increased in the ALl of rats but NariS lessened apoptosis and Fas protein expression in alveolar epithelial cells of rats with ALl. Conclusion Endogenous H2S protects rats from oleic acid-induced ALl, probably by inhibiting cell apoptosis.