Combined effects of maternal inflammation and neonatal hyperoxia on lung fibrosis and RAGE expression in newborn rats

Combined effects of maternal inflammation and neonatal hyperoxia on lung fibrosis and RAGE expression in newborn rats
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母体炎症和新生儿高氧对新生大鼠肺纤维化和RAGE表达的联合影响

DOI:
10.1038/pr.2013.222
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发表时间:
2014
期刊:
影响因子:
3.6
通讯作者:
Chung
Chung
中科院分区:
医学3区
文献类型:
--
作者:
C. Su;H. Chou;Liang;T. Yeh;Chung

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背景:晚期糖基化终产物受体(RAGE)与纤维化过程有关。我们假设由母体脂多糖(LPS)介导的炎症和新生儿高氧诱导的肺纤维化与新生大鼠的RAGE有关。方法:妊娠sd大鼠于妊娠第20、21天腹腔注射LPS或生理盐水(NS)。幼鼠饲养在室内空气(RA)或富含O2的环境(O2)中,分为NS + RA、NS + O2、LPS + RA和LPS + O2四个研究组。结果:lps注射组大鼠出生后第7天肺部干扰素-γ和白细胞介素-1β (IL-1β)水平明显高于ns注射组大鼠。高氧饲养的大鼠在出生后第7天的肺IL-10表达高于ra饲养的大鼠。LPS + O2组在出生后第7天和第21天总胶原蛋白和转化生长因子-β1含量显著高于NS+RA组。LPS + O2组在出生后第7天RAGE mRNA和sRAGE蛋白的表达显著低于NS+RA组。结论:RAGE可能参与了母体全身性炎症及产后高氧所致大鼠新生儿肺纤维化的发病机制。
Background:Receptors for advanced glycation end products (RAGE) have been implicated in fibrotic processes. We hypothesized that lung fibrosis induced by maternal lipopolysaccharide (LPS)-mediated inflammation and neonatal hyperoxia involves RAGE in newborn rats.Methods:Pregnant Sprague-Dawley rats received intraperitoneal injections of LPS or normal saline (NS) on 20 and 21 d of gestation. The pups were reared in room air (RA) or an O2-enrich atmosphere (O2), creating the four study groups, NS + RA, NS + O2, LPS + RA, and LPS + O2. The O2 treatment was >95% O2 for 7 d, followed by 60% O2 for 14 d.Results:Rat pups born to LPS-injected dams exhibited significantly higher lung interferon-γ and interleukin-1β (IL-1β) on postnatal day 7 than the pups born to NS-injected dams. Rat pups reared in hyperoxia expressed higher lung IL-10 on postnatal day 7, compared with the RA-reared pups. The LPS + O2 group had significantly higher total collagen and transforming growth factor-β1 on postnatal days 7 and 21 than the NS+RA group. RAGE mRNA and sRAGE protein expression were significantly lower in the LPS + O2 group on postnatal day 7 than the NS+RA group.Conclusion:RAGE may be involved in the pathogenesis of lung fibrosis induced by maternal systemic inflammation and postnatal hyperoxia in rat neonates.
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