title: Selenium Deficiency Facilitates Inflammation Through the Regulation of TLR4 and TLR4-Related Signaling Pathways in the Mice Uterus.
abstract: 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.
authors.affiliation: Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, 130062, , Jilin Province, People's Republic of China.
authors.forename: Zecai
authors.initials: Z
authors.lastname: Zhang
authors.forename: Xuejiao
authors.initials: X
authors.lastname: Gao
authors.forename: Yongguo
authors.initials: Y
authors.lastname: Cao
authors.forename: Haichao
authors.initials: H
authors.lastname: Jiang
authors.forename: Tiancheng
authors.initials: T
authors.lastname: Wang
authors.forename: Xiaojing
authors.initials: X
authors.lastname: Song
authors.forename: Mengyao
authors.initials: M
authors.lastname: Guo
authors.forename: Naisheng
authors.initials: N
authors.lastname: Zhang
mesh_terms: D000818:Animals; D004716:Endometritis / Q000139:chemically induced / Q000473:pathology*; D004797:Enzyme-Linked Immunosorbent Assay; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005260:Female; D020672:I-kappa B Proteins / Q000378:metabolism; D007249:Inflammation / Q000276:immunology*; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D008070:Lipopolysaccharides; D051379:Mice; D008807:Mice, Inbred BALB C; D000072000:NF-KappaB Inhibitor alpha; D010766:Phosphorylation; D012333:RNA, Messenger / Q000235:genetics; D011897:Random Allocation; D060888:Real-Time Polymerase Chain Reaction; D012643:Selenium / Q000172:deficiency* / Q000494:pharmacology; D015398:Signal Transduction; D013050:Spectrometry, Fluorescence; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism*; D051996:Transcription Factor RelA / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014599:Uterus / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D020672:I-kappa B Proteins; C587672:IL1B protein, mouse; D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; C000606205:Nfkbia protein, mouse; D012333:RNA, Messenger; C498144:Rela protein, mouse; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D000072000:NF-KappaB Inhibitor alpha; D048049:Extracellular Signal-Regulated MAP Kinases; D048031:JNK Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; D012643:Selenium