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Inhal Toxicol. 2015;27(12):613-20. doi: 10.3109/08958378.2015.1048909. Epub 2015 Oct 7.

Epithelial sodium channel is involved in H2S-induced acute pulmonary edema.

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a Department of Emergency Medicine , The First Affiliated Hospital of Nanjing Medical University , Nanjing , Jiangsu , P.R. China .
b Key Lab of Modern Toxicology (NJMU), Ministry of Education, Department of Toxicology, School of Public Health , Nanjing Medical University , Nanjing , Jiangsu , P.R. China , and.
c Department of Occupational Disease Prophylactic-Therapeutic Institution , Jiangsu Provincial Center for Disease Prevention and Control , Nanjing , Jiangsu , P.R. China.


Acute pulmonary edema is one of the major outcomes of exposure to high levels of hydrogen sulfide (H2S). However, the mechanisms involved in H2S-induced acute pulmonary edema are still poorly understood. Therefore, the present study is designed to evaluate the role of epithelial sodium channel (ENaC) in H2S-induced acute pulmonary edema. The Sprague-Dawley rats were exposed to sublethal concentrations of inhaled H2S, then the pulmonary histological and lung epithelial cell injury were evaluated by hematoxylin-eosin staining and electron microscopy, respectively. In addition to morphological investigation, our results also revealed that H2S exposure significantly decreased the alveolar fluid clearance and increased the lung tissue wet-dry ratio. These changes were demonstrated to be associated with decreased ENaC expression. Furthermore, the extracellular-regulated protein kinases 1/2 pathway was demonstrated to be implicated in H2S-mediated ENaC expression, because PD98059, an ERK1/2 antagonist, significantly mitigated H2S-mediated ENaC down-regulation. Therefore, our results show that ENaC might represent a novel pharmacological target for the treatment of acute pulmonary edema induced by H2S and other hazardous gases.


Acute pulmonary edema; ERK1/2; alveolar fluid clearance; epithelial sodium channel; hydrogen sulfide

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