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Oxidative Medicine and Cellular Longevity
Volume 2018, Article ID 9647809, 15 pages
https://doi.org/10.1155/2018/9647809
Research Article

Hydrogen Sulfide Alleviates Lipopolysaccharide-Induced Diaphragm Dysfunction in Rats by Reducing Apoptosis and Inflammation through ROS/MAPK and TLR4/NF-κB Signaling Pathways

1The First Affiliated Hospital of Henan University, Kaifeng, Henan 475001, China
2School of Basic Medical Sciences, Henan University College of Medicine, Kaifeng, Henan 475004, China
3Henan International Joint Laboratory for Nuclear Protein Regulation, Henan University, Kaifeng, Henan 475004, China
4College of Pharmacy, Henan University, Kaifeng, Henan 475004, China
5Huaihe Hospital of Henan University, Kaifeng, Henan 475000, China
6Brain Research Laboratory, College of Life Sciences, Henan University, Kaifeng, Henan 475004, China
7Department of Microbiology and Immunology, School of Medicine, University of Texas Medical Branch, Galveston, TX 77555, USA
8The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450014, China
9Henan Provincial People’s Hospital Affiliated to Henan University, Zhengzhou, Henan 450003, China

Correspondence should be addressed to Dong-Dong Wu; moc.anis@7002uwgnaygnod and Xin-Ying Ji; nc.ude.uneh@ij_gniynix

Received 25 January 2018; Revised 11 April 2018; Accepted 29 April 2018; Published 24 May 2018

Academic Editor: Eric E. Kelley

Copyright © 2018 Guo-Yu Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Diaphragm dysfunction is an important clinical problem worldwide. Hydrogen sulfide (H2S) is involved in many physiological and pathological processes in mammals. However, the effect and mechanism of H2S in diaphragm dysfunction have not been fully elucidated. In this study, we detected that the level of H2S was decreased in lipopolysaccharide- (LPS-) treated L6 cells. Treatment with H2S increased the proliferation and viability of LPS-treated L6 cells. We found that H2S decreased reactive oxygen species- (ROS-) induced apoptosis through the mitogen-activated protein kinase (MAPK) signaling pathway in LPS-treated L6 cells. Administration of H2S alleviated LPS-induced inflammation by mediating the toll-like receptor-4 (TLR-4)/nuclear factor-kappa B (NF-κB) signaling pathway in L6 cells. Furthermore, H2S improved diaphragmatic function and structure through the reduction of inflammation and apoptosis in the diaphragm of septic rats. In conclusion, these findings indicate that H2S ameliorates LPS-induced diaphragm dysfunction in rats by reducing apoptosis and inflammation through ROS/MAPK and TLR4/NF-κB signaling pathways. Novel slow-releasing H2S donors can be designed and applied for the treatment of diaphragm dysfunction.