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In AKI patients, levels of creatinine (Cre), urea nitrogen (BUN), tumor necrosis factor\u2010<jats:italic>\u03b1<\/jats:italic> (TNF\u2010<jats:italic>\u03b1<\/jats:italic>) and interleukin\u20101<jats:italic>\u03b2<\/jats:italic> (IL\u20101<jats:italic>\u03b2<\/jats:italic>), and myeloperoxidase (MPO) activity as well as concentrations of malondialdehyde (MDA) and hydrogen peroxide (H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>) were significantly increased compared with those of controls. However, plasma level of H<jats:sub>2<\/jats:sub>S 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 <jats:italic>in vivo<\/jats:italic> study. In AKI mice, H<jats:sub>2<\/jats:sub>S levels decreased with the decline of 3\u2010MST activity and expression; similar changes were observed in other indicators mentioned above. However, the protein expressions of TLR4, NLRP3, and caspase\u20101 in mice kidney tissues were significantly increased 6\u2009h after LPS injection. NaHS could improve renal function and kidney histopathological changes, attenuate LPS\u2010induced inflammation and oxidative stress, and inhibit expressions of TLR4, NLRP3, and caspase\u20101. Our study demonstrated that endogenous H<jats:sub>2<\/jats:sub>S is involved in the pathogenesis of SA\u2010AKI, and exogenous H<jats:sub>2<\/jats:sub>S exerts protective effects against LPS\u2010induced AKI by inhibiting inflammation and oxidative stress via the TLR4\/NLRP3 signaling pathway.<\/jats:p>","DOI":"10.1155\/2018\/6717212","type":"journal-article","created":{"date-parts":[[2018,1,31]],"date-time":"2018-01-31T23:38:18Z","timestamp":1517441898000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":112,"title":["Hydrogen Sulfide Attenuates LPS\u2010Induced Acute Kidney Injury by Inhibiting Inflammation and Oxidative 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