Epithelial sodium channel is involved in H2S-induced acute pulmonary edema.
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| Abstract |
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.
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| Authors | Lei Jiang, Yixin Wang, Chenglei Su, Hao Sun, Huazhong Zhang, Baoli Zhu, Hengdong Zhang, Hang Xiao, Jun Wang, Jinsong Zhang |
| Journal | Inhalation toxicology (Inhal Toxicol) Vol. 27 Issue 12 Pg. 613-20 ( 2015) ISSN: 1091-7691 [Electronic] England |
| PMID | 26444456 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't) |
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