期刊
INFLAMMATION
卷 41, 期 1, 页码 249-259出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-017-0684-4
关键词
acute lung injury; hydrogen sulfide; lipopolysaccharide; NADPHoxidase 2; reactive oxygen species
资金
- Deutsche Forschungsgemeinschaft (Bonn, Germany) [DFG HO 2464/3-1]
Acute lung injury (ALI) caused by septic stimuli is still a major problem in critical care patients. We have shown previously that hydrogen sulfide (H2S) mediates anti-inflammatory and lung protective effects. In the present study, we aimed to investigate the underlying mechanisms. C57BL/6N mice were instilled with lipopolysaccharide (LPS) intranasally in the absence or presence of inhaled H2S for 6 h. LPS instillation led to alveolar wall thickening, an elevated ALI score, increased neutrophil transmigration, and elevated interleukin-1 beta cytokine release into the bronchoalveolar lavage fluid. In contrast, H2S inhalation prevented lung injury and inflammation despite LPS treatment. Moreover, H2S inhalation significantly inhibited protein expression of cystathionine-beta-synthetase, heat shock protein 70, phosphorylated p38 MAP kinase, NADPH oxidase 2, and the formation of reactive oxygen species (ROS) in LPS-challenged animals. In conclusion, H2S prevents LPS-induced ALI by inhibition of pro-inflammatory and oxidative responses via the concerted attenuation of stress protein, MAP kinase, and ROS signaling pathways.
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