Selenium Inhibits LPS-Induced Pro-inflammatory Gene Expression by Modulating MAPK and NF-κB Signaling Pathways in Mouse Mammary Epithelial Cells in Primary Culture

• DOI: 10.1007/s10753-013-9761-5
• Publication Date: 2013-11-07T08:39:46Z
• Authors: Wen Zhang; Runxiang Zhang; Tiancheng Wang; Haichao Jiang; Mengyao Guo; Ershun Zhou; Yong Sun; Zhengtao Yang; Shiwen Xu; Yongguo Cao; Naisheng Zhang
• Keywords: Lipopolysaccharides; 2. Zero hunger; 0303 health sciences; Dose-Response Relationship, Drug; Primary Cell Culture; Anti-Inflammatory Agents; NF-kappa B; Mastitis; 3. Good health; Enzyme Activation; Mice; 03 medical and health sciences; Mammary Glands, Animal; Gene Expression Regulation; Cyclooxygenase 2; Pregnancy; Animals; Female; I-kappa B Proteins; Inflammation Mediators; Mitogen-Activated Protein Kinases; Phosphorylation; Cells, Cultured; Signal Transduction

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.