Regulatory effects of hydrogen sulfide on alveolar epithelial cell endoplasmic reticulum stress in rats with acute lung injury
10.5847/wjem.j.1920-8642.2015.01.012
- Author:
Zhi-Wei LIU
1
;
Hai-Ying WANG
;
Lan GUAN
;
Bin ZHAO
Author Information
1. Department of Emergency Medicine
- Publication Type:Journal Article
- Keywords:
Hydrogen sulfide;
Acute lung injury;
Endoplasmic reticulum stress
- From:
World Journal of Emergency Medicine
2015;6(1):67-73
- CountryChina
- Language:English
-
Abstract:
BACKGROUND: The present study was undertaken to examine the regulatory effect of hydrogen sulfide (H2S) on endoplasmic reticulum stress in alveolar epithelial cells of rats with acute lung injury (ALI) induced by oleic acid (OA). METHODS: Seventy-two male Sprague Dawley (SD) rats were divided into control group, oleic acid-induced ALI group (OA group), oleic acid-induced ALI with sodium hydrosulfide (NaHS) pretreatment group (OA+NaHS group), and sodium hydrosulfide treatment group (NaHS group). Rats of each group were further subdivided into 3 subgroups. Index of quantitative assessment of histological lung injury (IQA), wet/dry weight ratio (W/D) and H2S level of lung tissues were measured. The expressions of endoplasmic reticulum stress markers including glucose-regulated protein 78 (GRP78) and α-subunit of eukaryotic translation initiation factor-2 (elF2α) in lung tissues were measured by immunohistochemical staining and Western blotting. RESULTS: The IQA score and W/D ratio of lung tissues at the three time points significantly increased in rats injected with OA, but significantly decreased in other rats injected with OA and NaHS. The level of H2S in lung tissue at the three time points significantly decreased in rats injected with OA, but significantly increased in other rats injected with both OA and NaHS. GRP78 and elF2αdecreased in rats injected with OA, but increased in other rats injected with both OA and NaHS, especially at 4-hour and 6-hour time points. CONCLUSION: The results suggested that H2S could promote alveolar epithelial cell endoplasmic reticulum stress in rats with ALI.
