title: Selenium inhibits LPS-induced pro-inflammatory gene expression by modulating MAPK and NF-κB signaling pathways in mouse mammary epithelial cells in primary culture.
abstract: Mastitis is characterized by an inflammation of the mammary gland of dairy animals and humans; this condition is one of the major causes of economic losses in dairy industries. Selenium (Se), a biological trace element, modulates the functions of many regulatory proteins in signal transduction and provides advantages for animals with inflammatory diseases, including mastitis. The current study aimed to assess the protective effects and the active mechanism of Na(2)SeO(3) against lipopolysaccharide (LPS)-induced inflammation in mouse mammary epithelial cells (MMECs). Our results showed that LPS-induced expressions of cyclooxygenase-2 and tumor necrosis factor-α significantly decreased after Se was supplemented to Se-deficient MMECs. Na(2)SeO(3) also suppressed LPS-induced nuclear factor-κB activation, inhibitory kappa B degradation, and ERK, JNK, and P38 phosphorylation in a dose-dependent manner. These results suggested that Se functions as an anti-inflammatory agent in mastitis.
authors.affiliation: Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, 130062, Jilin, People's Republic of China.
authors.forename: Wen
authors.initials: W
authors.lastname: Zhang
authors.forename: Runxiang
authors.initials: R
authors.lastname: Zhang
authors.forename: Tiancheng
authors.initials: T
authors.lastname: Wang
authors.forename: Haichao
authors.initials: H
authors.lastname: Jiang
authors.forename: Mengyao
authors.initials: M
authors.lastname: Guo
authors.forename: Ershun
authors.initials: E
authors.lastname: Zhou
authors.forename: Yong
authors.initials: Y
authors.lastname: Sun
authors.forename: Zhengtao
authors.initials: Z
authors.lastname: Yang
authors.forename: Shiwen
authors.initials: S
authors.lastname: Xu
authors.forename: Yongguo
authors.initials: Y
authors.lastname: Cao
authors.forename: Naisheng
authors.initials: N
authors.lastname: Zhang
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002478:Cells, Cultured; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004789:Enzyme Activation; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D020672:I-kappa B Proteins / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008321:Mammary Glands, Animal / Q000187:drug effects* / Q000201:enzymology / Q000276:immunology; D008413:Mastitis / Q000201:enzymology / Q000235:genetics / Q000276:immunology / Q000517:prevention & control*; D051379:Mice; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D016328:NF-kappa B / Q000378:metabolism*; D010766:Phosphorylation; D011247:Pregnancy; D061251:Primary Cell Culture; D015398:Signal Transduction / Q000187:drug effects*; D018038:Sodium Selenite / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D020672:I-kappa B Proteins; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D020928:Mitogen-Activated Protein Kinases; D018038:Sodium Selenite