Selenium Deficiency Facilitates Inflammation Through the Regulation of TLR4 and TLR4-Related Signaling Pathways in the Mice Uterus

Selenium Deficiency Facilitates Inflammation Through the Regulation of TLR4 and TLR4-Related Signaling Pathways in the Mice Uterus
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缺硒通过调节小鼠子宫中的 TLR4 和 TLR4 相关信号通路促进炎症

DOI:
10.1007/s10753-014-0106-9
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发表时间:
2015-01
期刊:
影响因子:
5.1
通讯作者:
Zhang, Naisheng
Zhang, Naisheng
中科院分区:
医学2区
文献类型:
--
作者:
Wang, Tiancheng;Song, Xiaojing;Guo, Mengyao;Zhang, Naisheng

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硒(Se)是一种重要的微量营养元素,影响生殖系统的发育和功能。子宫内膜炎是一种严重影响动物繁殖能力的生殖障碍性疾病。为研究硒缺乏对脂多糖(LPS)诱导的小鼠肠炎的影响,建立了LPS诱导的小鼠肠炎模型。用荧光分光光度法测定子宫组织中硒的含量。采用酶联免疫吸附试验(ELISA)和实时定量聚合酶链反应(qRT-PCR)测定肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-1β和IL-6水平。Western blot检测IκBα、NF-κB p65、ERK、JNK和p38的磷酸化程度及Toll样受体4(TLR 4)的表达。用qRT-PCR分析TLR 4信使RNA(mRNA)。结果表明,日粮硒摄入量显著影响子宫组织硒水平。结果表明,低硒可导致LPS诱导的小鼠子宫内膜炎的病理改变,TNF-α、IL-1β、IL-6的表达增加,TLR 4的活化增强,IκBα、p65、ERK、JNK、p38的磷酸化水平升高。补充硒可抑制上述作用。总之,我们的研究表明,硒缺乏使小鼠子宫更容易发生炎症。适当补硒可提高子宫免疫功能。
Selenium (Se) is an essential nutritional trace element that affects the development and function of the reproductive system. Endometritis is a reproductive obstacle disease that can seriously reduce the reproductive capacity of animal. To study the effects of dietary Se deficiency on lipopolysaccharide (LPS)-induced mice endometritis, we generated a model of LPS-induced mice endometritis. The Se content in uterine tissues was detected by fluorescence spectrophotometry. The levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 were measured by enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR). The extent of phosphorylation of IκBα, NF-κB p65, ERK, JNK, and p38 and the expression of Toll-like receptor 4 (TLR4) were detected with Western blots. The TLR4 messenger RNA (mRNA) was analyzed with qRT-PCR. The results indicated that dietary Se intake significantly influenced Se levels in uterine tissues. The Se-deficient mice model was successfully replicated, and Se deficiency exacerbated uterine tissue histopathology; increased the expression of TNF-α, IL-1β, and IL-6; facilitated the activation of TLR4; and enhanced the phosphorylation of IκBα, p65, ERK, JNK, and p38 in LPS-induced mice endometritis. Also, the effects were inhibited by a supplement of Se. In conclusion, our studies demonstrated that Se deficiency makes mice uterus more prone to inflammation. An appropriate Se supplement could enhance the immune condition of the uterus.
DOI: 10.1007/978-3-642-80186-0_7
发表时间: 1996
影响因子: --
作者:
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DOI: 10.3181/00379727-182-42361
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DOI: 10.1007/s10753-013-9761-5
发表时间: 2014-04-01
期刊: INFLAMMATION
影响因子: 5.1
作者:
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DOI: 10.1007/s10753-014-9925-y
发表时间: 2014-05
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作者:
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