Hydrogen Sulfide Attenuates LPS-Induced Acute Kidney Injury by Inhibiting Inflammation and Oxidative Stress.
Hydrogen Sulfide Attenuates LPS-Induced Acute Kidney Injury by Inhibiting Inflammation and Oxidative Stress.
复制标题
硫化氢通过抑制炎症和氧化应激减轻脂多糖引起的急性肾损伤
DOI：
10.1155/2018/6717212
复制
发表时间：
2018
影响因子：
--
通讯作者：
Wu Y
中科院分区：
文献类型：
--
作者：
Chen Y;Jin S;Teng X;Hu Z;Zhang Z;Qiu X;Tian D;Wu Y
为探讨硫化氢（H2S）在脓毒症相关急性肾损伤（SA-AKI）中的保护机制，入选了10例阿基患者和10例健康对照。阿基患者血清肌酐（Cre）、尿素氮（BUN）、肿瘤坏死因子-α（TNF-α）、白细胞介素-1 β（IL-1β）、髓过氧化物酶（MPO）活性、丙二醛（MDA）和过氧化氢（H2 O2）浓度均显著高于对照组。而血浆H2S水平降低，并与Cre、BUN水平呈线性相关。然后，通过腹腔内注射脂多糖（LPS）构建阿基小鼠模型用于体内研究。在阿基小鼠中，H2S水平随着3-MST活性和表达的下降而下降;上述其他指标也观察到类似的变化。LPS注射后6 h，小鼠肾组织中TLR 4、NLRP 3和caspase-1的蛋白表达显著增加。NaHS可改善肾功能和肾脏组织病理学改变，减轻LPS诱导的炎症反应和氧化应激，抑制TLR 4、NLRP 3和caspase-1的表达。我们的研究表明，内源性H2S参与SA-AKI的发病机制，外源性H2S通过TLR 4/NLRP 3信号通路抑制炎症和氧化应激而对LPS诱导的阿基发挥保护作用。
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.
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DOI：
10.1097/shk.0000000000000478
发表时间：
2016-01
期刊：
Shock (Augusta, Ga.)
影响因子：
--
作者：
Ahmad A;Olah G;Szczesny B;Wood ME;Whiteman M;Szabo C
通讯作者：
Szabo C
影响因子：
--
作者：
Avanzato, Daniele;Merlino, Annalisa;Mancardi, Daniele
通讯作者：
Mancardi, Daniele
影响因子：
19.6
作者：
Kim, Duk Hoon;Jung, Yu Jin;Kim, Won
通讯作者：
Kim, Won
影响因子：
4.4
作者：
Cunningham, PN;Wang, Y;Quigg, RJ
通讯作者：
Quigg, RJ
老年糖尿病小鼠心脏 H2S 生成量减少。
影响因子：
--
作者：
Jin S;Pu SX;Hou CL;Ma FF;Li N;Li XH;Tan B;Tao BB;Wang MJ;Zhu YC
通讯作者：
Zhu YC