Hydrogen Sulfide Delays LPS-Induced Preterm Birth in Mice via Anti-Inflammatory Pathways.
Hydrogen Sulfide Delays LPS-Induced Preterm Birth in Mice via Anti-Inflammatory Pathways.
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硫化氢通过抗炎途径延迟 LPS 诱导的小鼠早产
DOI：
10.1371/journal.pone.0152838
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Ni X
中科院分区：
文献类型：
--
作者：
Liu W;Xu C;You X;Olson DM;Chemtob S;Gao L;Ni X
孕妇早产的一个主要原因是羊膜内感染，这是由炎症过程介导的。硫化氢（H2S）是一种气态递质，与炎症反应有关。我们试图通过脂多糖（LPS）诱导的早产小鼠模型来研究H2S是否影响感染性早产。妊娠14.5天，腹腔注射LPS (0.4 mg/kg) 2次，诱导早产。LPS显著增加子宫内白细胞浸润，刺激子宫肌层促炎因子白细胞介素1β (IL-1β)、IL-6、肿瘤坏死因子α (TNF-α)、CCL2、CXCL15的表达。NaHS （i.p.）的使用以剂量依赖的方式延迟LPS诱导的分娩发生。NaHS可阻止白细胞向宫内组织浸润，抑制子宫肌层中促炎细胞因子的产生，并降低母体循环中这些细胞因子的水平。H2S还降低了肌层中脂多糖激活的细胞外信号调节激酶（ERK） 1/2/核因子(NF)-κB信号通路。该研究为H2S在减轻炎症中的作用提供了新的体内证据，并为感染相关性早产提供了潜在的新治疗策略。
A major cause of preterm labor in pregnant women is intra-amniotic infection, which is mediated by an inflammatory process. Hydrogen sulfide (H2S), a gaseous transmitter, has been implicated to be involved in inflammatory responses. We sought to investigate whether H2S affects infectious preterm birth using the mouse model of lipopolysaccharides (LPS)-induced preterm birth. Administration of LPS at 0.4 mg/kg with two injections intraperitoneally (i.p.) on gestational day 14.5 induced preterm labor. LPS significantly increased leukocyte infiltration in uterus, stimulated the expression of pro-inflammatory cytokines interleukin 1β (IL-1β), IL-6, tumor necrosis factor α (TNF-α), CCL2 and CXCL15 in myometrium. Administration of NaHS (i.p.) delayed the onset of labor induced by LPS in a dose-dependent manner. NaHS prevented leukocyte infiltration into intrauterine tissues and inhibited the production of pro-inflammatory cytokines in myometrium and decreased the levels of these cytokines in maternal circulation. H2S also decreased LPS-activated extracellular signal-regulated kinase (ERK) 1/2/ nuclear factor (NF)-κB signaling pathways in myometrium. This study provides new in vivo evidence for the roles of H2S in attenuating inflammation, and a potential novel therapeutic strategy for infection-related preterm labor.