In:
Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2018 ( 2018), p. 1-15
Abstract:
Diaphragm dysfunction is an important clinical problem worldwide. Hydrogen sulfide (H 2 S) is involved in many physiological and pathological processes in mammals. However, the effect and mechanism of H 2 S in diaphragm dysfunction have not been fully elucidated. In this study, we detected that the level of H 2 S was decreased in lipopolysaccharide- (LPS-) treated L6 cells. Treatment with H 2 S increased the proliferation and viability of LPS-treated L6 cells. We found that H 2 S decreased reactive oxygen species- (ROS-) induced apoptosis through the mitogen-activated protein kinase (MAPK) signaling pathway in LPS-treated L6 cells. Administration of H 2 S alleviated LPS-induced inflammation by mediating the toll-like receptor-4 (TLR-4)/nuclear factor-kappa B (NF- κ B) signaling pathway in L6 cells. Furthermore, H 2 S improved diaphragmatic function and structure through the reduction of inflammation and apoptosis in the diaphragm of septic rats. In conclusion, these findings indicate that H 2 S ameliorates LPS-induced diaphragm dysfunction in rats by reducing apoptosis and inflammation through ROS/MAPK and TLR4/NF- κ B signaling pathways. Novel slow-releasing H 2 S donors can be designed and applied for the treatment of diaphragm dysfunction.
Type of Medium:
Online Resource
ISSN:
1942-0900
,
1942-0994
DOI:
10.1155/2018/9647809
Language:
English
Publisher:
Hindawi Limited
Publication Date:
2018
detail.hit.zdb_id:
2455981-7
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