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Oxidative Medicine and Cellular Longevity
Volume 2018 (2018), Article ID 6717212, 10 pages
Research Article

Hydrogen Sulfide Attenuates LPS-Induced Acute Kidney Injury by Inhibiting Inflammation and Oxidative Stress

1Department of Physiology, Hebei Medical University, Hebei, China
2Intensive Care Unit, The Fourth Hospital of Hebei Medical University, Hebei, China
3Department of Endocrinology, The Third Hospital of Hebei Medical University, Hebei, China
4Hebei Collaborative Innovation Center for Cardio-Cerebrovascular Disease, Hebei, China
5Key Laboratory of Vascular Medicine of Hebei Province, Hebei, China

Correspondence should be addressed to Yuming Wu

Received 27 August 2017; Revised 21 November 2017; Accepted 4 December 2017; Published 31 January 2018

Academic Editor: Mohamed A. Abdelmegeed

Copyright © 2018 Yuhong Chen 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.


In order to investigate the protective mechanism of hydrogen sulfide (H2S) in sepsis-associated acute kidney injury (SA-AKI), ten AKI patients and ten healthy controls were enrolled. In AKI patients, levels of creatinine (Cre), urea nitrogen (BUN), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and myeloperoxidase (MPO) activity as well as concentrations of malondialdehyde (MDA) and hydrogen peroxide (H2O2) were significantly increased compared with those of controls. However, plasma level of H2S decreased and was linearly correlated with levels of Cre and BUN. After that, an AKI mouse model by intraperitoneal lipopolysaccharide (LPS) injection was constructed for in vivo study. In AKI mice, H2S levels decreased with the decline of 3-MST activity and expression; similar changes were observed in other indicators mentioned above. However, the protein expressions of TLR4, NLRP3, and caspase-1 in mice kidney tissues were significantly increased 6 h after LPS injection. NaHS could improve renal function and kidney histopathological changes, attenuate LPS-induced inflammation and oxidative stress, and inhibit expressions of TLR4, NLRP3, and caspase-1. Our study demonstrated that endogenous H2S is involved in the pathogenesis of SA-AKI, and exogenous H2S exerts protective effects against LPS-induced AKI by inhibiting inflammation and oxidative stress via the TLR4/NLRP3 signaling pathway.