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

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• 作者：Zecai Zhang ; Xuejiao Gao ; Yongguo Cao ; Haichao Jiang ; Tiancheng Wang…
• 关键词：selenium ; endometritis ; TLR4 ; inflammation ; signaling pathway
• 刊名：Inflammation
• 出版年：2015
• 出版时间：June 2015
• 年：2015
• 卷：38
• 期：3
• 页码：1347-1356
• 全文大小：1,546 KB
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  23.Guo
• 作者单位：Zecai Zhang (1)
  Xuejiao Gao (1)
  Yongguo Cao (1)
  Haichao Jiang (1)
  Tiancheng Wang (1)
  Xiaojing Song (1)
  Mengyao Guo (2)
  Naisheng Zhang (1)
  
  1. Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, 130062,, Jilin Province, People’s Republic of China
  2. College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, People’s Republic of China
  
• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Rheumatology
  Internal Medicine
  Pharmacology and Toxicology
  Pathology
  
• 出版者：Springer Netherlands
• ISSN：1573-2576

文摘

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.