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The therapeutic mechanism of dexamethasone in lung injury induced by hydrogen sulfide


1 Department of Emergency Medicine, Changshu Hospital Affiliated to Soochow University, The First People’s Hospital of Changshu, Changshu, 215500, China
2 Department of Emergency Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China
3 The Department of Oncology, The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital and Jiangsu Institute of Cancer Research, Nanjing, 210000, China
4 Key Lab of Modern Toxicology, Ministry of Education, Department of Toxicology, School of Public Health, Nanjing Medical University, Nanjing, 211166, China

* Corresponding Authors: HONGWEI YE. Email: email; BO CHEN. Email: email

BIOCELL 2023, 47(9), 2027-2035.


Background: The lung is one of the primary target organs of hydrogen sulfide (H2S), as exposure to H2S can cause acute lung injury (ALI) and pulmonary edema. Dexamethasone (Dex) exerts a protective effect on ALI caused by exposure to toxic gases and is commonly used in the clinic; however, the underlying mechanisms remain elusive, and the dose is unclear. Methods: In vivo experiments: divided C57BL6 mice into 6 groups at random, 12 in each group. The mice were exposed to H2S for 3 h and 5 or 50 mg/kg Dex pretreated before exposure, sacrificed 12 h later. The morphological changes of HE staining and the ultrastructural changes of lungs under transmission electron microscopy were evaluated. The wet/dry ratio of lung tissue was measured. Bronchial alveolar lavage fluid (BALF) protein content and lung permeability index were detected. The expression of AQP5 protein was measured by immunohistochemistry and Western Blot (WB). In vitro experiments: divided human lung adenocarcinoma cell line A549 into 4 groups. 1 μmol/L dexamethasone was added to pre-incubation. The WB analyzed the protein of p-ERK1/2, p-JNK, and p-p38 in MAPK pathway after 1 h of NaHS exposure; six hours after NaHS exposure, the AQP5 protein was measured by WB. Results: Dex treatment could significantly attenuate the H2S-induced destruction to the alveolar wall, increase the wet-to-dry weight ratio and decrease pulmonary permeability index, with high-dose dexamethasone seemingly functioning better. Additionally, our previous studies showed that aquaporin 5 (AQP 5), a critical protein that regulates water flux, decreased both in a mouse and cell model following the exposure to H2S. This study indicates that tThe decrease in AQP 5 can be alleviated by Dex treatment. Additionally, the mitogen activated protein kinase (MAPK) pathway may be involved in the protective effects of Dex in ALI caused by exposure to H2S since H2S-induced MAPK activation could be inhibited by Dex. Conclusion: The present results indicate that AQP 5 may be considered a therapeutic target for Dex in H2S or other hazardous gases-induced ALI.


Cite This Article

XU, C., YANG, C., ZHANG, J., PAN, X., WANG, J. et al. (2023). The therapeutic mechanism of dexamethasone in lung injury induced by hydrogen sulfide. BIOCELL, 47(9), 2027–2035.

cc This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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