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组织学绒毛膜羊膜炎不会调节自发性早产妊娠中的氧化应激和抗氧化状态。

Histologic chorioamnionitis does not modulate the oxidative stress and antioxidant status in pregnancies complicated by spontaneous preterm delivery.

机构信息

Department of Pathology, Botucatu Medical School, São Paulo State University (UNESP), Distrito de Rubião Júnior, Botucatu, São Paulo, CEP 18618-686, Brazil.

Department of Gynecology and Obstetrics, Federal University of Paraíba, UFPB, João Pessoa, Brazil.

出版信息

BMC Pregnancy Childbirth. 2017 Nov 13;17(1):376. doi: 10.1186/s12884-017-1549-4.

DOI:10.1186/s12884-017-1549-4
PMID:29132320
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5684743/
Abstract

BACKGROUND

Infection induced-inflammation and other risk factors for spontaneous preterm birth (PTB) and preterm premature rupture of membranes (pPROM) may cause a redox imbalance, increasing the release of free radicals and consuming antioxidant defenses. Oxidative stress, in turn, can initiate intracellular signaling cascades that increase the production of pro-inflammatory mediators. The objective of this study was to evaluate the oxidative damage to proteins and antioxidant capacity profiles in amniochorion membranes from preterm birth (PTB) and preterm premature rupture of membranes (pPROM) and to determine the role of histologic chorioamnionitis in this scenario.

METHODS

We included 27 pregnant women with PTB, 27 pPROM and 30 at term. Protein oxidative damage was assayed by 3-nitrotyrosine (3-NT) and carbonyl levels, using enzyme-linked immunosorbent assay (ELISA) and modified dinitrophenylhydrazine assay (DNPH), respectively. Total antioxidant capacity (TAC) was measured by ELISA.

RESULTS

Protein oxidative damage determined by carbonyl levels was lower in PTB group than pPROM and term groups (p < 0.001). PTB group presented higher TAC compared with pPROM and term groups (p = 0.002). Histologic chorioamnionitis did not change either protein oxidative damage or TAC regardless of gestational outcome.

CONCLUSION

These results corroborates previous reports that pPROM and term birth exhibit similarities in oxidative stress- induced senescence and histologic chorioamnionitis does not modulate oxidative stress or antioxidant status.

摘要

背景

感染引起的炎症和其他自发性早产 (PTB) 和早产胎膜早破 (pPROM) 的风险因素可能导致氧化还原失衡,增加自由基的释放并消耗抗氧化防御。氧化应激反过来又可以引发细胞内信号级联反应,增加促炎介质的产生。本研究的目的是评估早产 (PTB) 和早产胎膜早破 (pPROM) 羊膜绒毛膜中蛋白质的氧化损伤和抗氧化能力谱,并确定组织学绒毛膜羊膜炎在这种情况下的作用。

方法

我们纳入了 27 名 PTB 孕妇、27 名 pPROM 孕妇和 30 名足月孕妇。使用酶联免疫吸附试验 (ELISA) 和改良的二硝基苯肼试验 (DNPH) 分别通过 3-硝基酪氨酸 (3-NT) 和羰基水平测定蛋白质氧化损伤。使用 ELISA 测定总抗氧化能力 (TAC)。

结果

通过羰基水平测定的蛋白质氧化损伤在 PTB 组低于 pPROM 组和足月组 (p<0.001)。PTB 组的 TAC 高于 pPROM 组和足月组 (p=0.002)。无论妊娠结局如何,组织学绒毛膜羊膜炎均未改变蛋白质氧化损伤或 TAC。

结论

这些结果证实了先前的报告,即 pPROM 和足月分娩在氧化应激诱导的衰老方面具有相似性,组织学绒毛膜羊膜炎不会调节氧化应激或抗氧化状态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/5684743/e52c862e149b/12884_2017_1549_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/5684743/f21b5e3f7c3b/12884_2017_1549_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/5684743/e52c862e149b/12884_2017_1549_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/5684743/f21b5e3f7c3b/12884_2017_1549_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39c4/5684743/e52c862e149b/12884_2017_1549_Fig2_HTML.jpg

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