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In vitro selenium supplementation suppresses key mediators involved in myometrial activation and rupture of fetal membranes.
Metallomics ( IF 2.9 ) Pub Date : 2020-04-29 , DOI: 10.1039/d0mt00063a Dineli Matheesha Kalansuriya 1 , Ratana Lim 2 , Martha Lappas 2
Metallomics ( IF 2.9 ) Pub Date : 2020-04-29 , DOI: 10.1039/d0mt00063a Dineli Matheesha Kalansuriya 1 , Ratana Lim 2 , Martha Lappas 2
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Spontaneous preterm birth, which can affect up to 20% of all pregnancies, is the greatest contributor to perinatal morbidity and mortality. Infection is the leading pathological cause of spontaneous preterm birth. Infection activates the maternal immune system, resulting in the upregulation of pro-inflammatory and pro-labor mediators that activate myometrial contractions and rupture of fetal membranes. Anti-inflammatory agents therefore have the potential for the prevention of spontaneous preterm birth. Selenium, an essential micronutrient, has been shown to be a potent anti-inflammatory regulator. Notably, clinical and epidemiological studies have suggested a link between selenium and preterm birth. Thus, the aim of this study was to assess the effect of selenite (an inorganic form of selenium) on the expression of pro-inflammatory and pro-labor mediators in human gestational tissues. Human fetal membranes and myometrium were pre-incubated with or without selenite before incubation with the bacterial product lipopolysaccharide (LPS) to stimulate inflammation associated with preterm birth. Selenite blocked LPS-induced expression of pro-inflammatory cytokines and chemokines and enzymes involved in remodelling of myometrium and degradation of fetal membranes. Of note, selenite also suppressed myometrial activation induced by inflammation as evidenced by a decrease in LPS-induced prostaglandin signalling and myometrial cell contractility. These effects of selenite were mediated by the MAPK protein ERK as selenite blunted LPS induced activation of ERK. In conclusion, selenite suppresses key mediators involved in inflammation induced activation of mediators involved in active labor in human fetal membranes and myometrium. These findings support recent clinical studies demonstrating selenium supplementation is associated with decreased incidence of spontaneous preterm birth.
中文翻译：
体外补充硒可抑制参与子宫肌层激活和胎膜破裂的关键介质。
自发性早产可影响多达 20% 的妊娠，是围产期发病率和死亡率的最大原因。感染是自然早产的主要病理原因。感染会激活母体免疫系统，导致促炎和促分娩介质上调，从而激活子宫肌层收缩和胎膜破裂。因此，抗炎剂具有预防自发性早产的潜力。硒是一种必需的微量营养素，已被证明是一种有效的抗炎调节剂。值得注意的是，临床和流行病学研究表明硒与早产之间存在联系。因此，本研究的目的是评估亚硒酸盐（一种无机形式的硒）对人类妊娠组织中促炎和促分娩介质表达的影响。在与细菌产物脂多糖 (LPS) 孵育之前，将人类胎膜和子宫肌层与或不与亚硒酸盐预孵育，以刺激与早产相关的炎症。亚硒酸盐阻止 LPS 诱导的促炎细胞因子和趋化因子以及参与子宫肌层重塑和胎膜降解的酶的表达。值得注意的是，亚硒酸盐还抑制了炎症诱导的子宫肌层激活，这可以通过 LPS 诱导的前列腺素信号传导和子宫肌层细胞收缩力的减少来证明。亚硒酸盐的这些作用是由 MAPK 蛋白 ERK 介导的，因为亚硒酸盐钝化 LPS 诱导了 ERK 的激活。总之，亚硒酸盐抑制了参与炎症诱导激活的关键介质，这些介质参与了人胎膜和子宫肌层的主动分娩。这些发现支持最近的临床研究，证明补充硒与降低自发性早产的发生率有关。
更新日期：2020-06-25
中文翻译：
体外补充硒可抑制参与子宫肌层激活和胎膜破裂的关键介质。
自发性早产可影响多达 20% 的妊娠，是围产期发病率和死亡率的最大原因。感染是自然早产的主要病理原因。感染会激活母体免疫系统，导致促炎和促分娩介质上调，从而激活子宫肌层收缩和胎膜破裂。因此，抗炎剂具有预防自发性早产的潜力。硒是一种必需的微量营养素，已被证明是一种有效的抗炎调节剂。值得注意的是，临床和流行病学研究表明硒与早产之间存在联系。因此，本研究的目的是评估亚硒酸盐（一种无机形式的硒）对人类妊娠组织中促炎和促分娩介质表达的影响。在与细菌产物脂多糖 (LPS) 孵育之前，将人类胎膜和子宫肌层与或不与亚硒酸盐预孵育，以刺激与早产相关的炎症。亚硒酸盐阻止 LPS 诱导的促炎细胞因子和趋化因子以及参与子宫肌层重塑和胎膜降解的酶的表达。值得注意的是，亚硒酸盐还抑制了炎症诱导的子宫肌层激活，这可以通过 LPS 诱导的前列腺素信号传导和子宫肌层细胞收缩力的减少来证明。亚硒酸盐的这些作用是由 MAPK 蛋白 ERK 介导的，因为亚硒酸盐钝化 LPS 诱导了 ERK 的激活。总之，亚硒酸盐抑制了参与炎症诱导激活的关键介质，这些介质参与了人胎膜和子宫肌层的主动分娩。这些发现支持最近的临床研究，证明补充硒与降低自发性早产的发生率有关。
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