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2018 ; 2018
(ä): 6717212
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Hydrogen Sulfide Attenuates LPS-Induced Acute Kidney Injury by Inhibiting
Inflammation and Oxidative Stress
#MMPMID29636853
Chen Y
; Jin S
; Teng X
; Hu Z
; Zhang Z
; Qiu X
; Tian D
; Wu Y
Oxid Med Cell Longev
2018[]; 2018
(ä): 6717212
PMID29636853
show ga
In order to investigate the protective mechanism of hydrogen sulfide (H(2)S) 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-? (TNF-?) and interleukin-1? (IL-1?), and
myeloperoxidase (MPO) activity as well as concentrations of malondialdehyde (MDA)
and hydrogen peroxide (H(2)O(2)) were significantly increased compared with those
of controls. However, plasma level of H(2)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 in vivo study. In AKI
mice, H(2)S 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 H(2)S is involved in the pathogenesis of
SA-AKI, and exogenous H(2)S exerts protective effects against LPS-induced AKI by
inhibiting inflammation and oxidative stress via the TLR4/NLRP3 signaling
pathway.