TY - JOUR
T1 - Hydrogen sulfide delays LPS-Induced preterm birth in mice via anti-inflammatory pathways
AU - Liu, Weina
AU - Xu, Chen
AU - You, Xingji
AU - Olson, David M.
AU - Chemtob, Sylvain
AU - Gao, Lu
AU - Ni, Xin
N1 - Publisher Copyright:
© 2016 Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2016/4
Y1 - 2016/4
N2 - A major cause of preterm labor in pregnant women is intra-amniotic infection, which is mediated by an inflammatory process. Hydrogen sulfide (H2 S), a gaseous transmitter, has been implicated to be involved in inflammatory responses. We sought to investigate whether H2 S 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 dosedependent 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. H2 S also decreased LPS-activated extracellular signal-regulated kinase (ERK) 1/2/ nuclear factor (NF)-êB signaling pathways in myometrium. This study provides new in vivo evidence for the roles of H2 S in attenuating inflammation, and a potential novel therapeutic strategy for infection-related preterm labor.
AB - A major cause of preterm labor in pregnant women is intra-amniotic infection, which is mediated by an inflammatory process. Hydrogen sulfide (H2 S), a gaseous transmitter, has been implicated to be involved in inflammatory responses. We sought to investigate whether H2 S 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 dosedependent 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. H2 S also decreased LPS-activated extracellular signal-regulated kinase (ERK) 1/2/ nuclear factor (NF)-êB signaling pathways in myometrium. This study provides new in vivo evidence for the roles of H2 S in attenuating inflammation, and a potential novel therapeutic strategy for infection-related preterm labor.
UR - https://www.scopus.com/pages/publications/84962641201
U2 - 10.1371/journal.pone.0152838
DO - 10.1371/journal.pone.0152838
M3 - 文章
C2 - 27035826
AN - SCOPUS:84962641201
SN - 1932-6203
VL - 11
JO - PLoS ONE
JF - PLoS ONE
IS - 4
M1 - e0152838
ER -