Selenium inhibits LPS-induced pro-inflammatory gene expression by modulating MAPK and NF-κB signaling pathways in mouse mammary epithelial cells in primary culture

Wen Zhang; Runxiang Zhang; Tiancheng Wang; Haichao Jiang; Mengyao Guo; Ershun Zhou; Yong Sun; Zhengtao Yang; Shiwen Xu; Yongguo Cao; Naisheng Zhang

doi:10.1007/s10753-013-9761-5

Selenium inhibits LPS-induced pro-inflammatory gene expression by modulating MAPK and NF-κB signaling pathways in mouse mammary epithelial cells in primary culture

Inflammation. 2014 Apr;37(2):478-85. doi: 10.1007/s10753-013-9761-5.

Authors

Wen Zhang¹, Runxiang Zhang, Tiancheng Wang, Haichao Jiang, Mengyao Guo, Ershun Zhou, Yong Sun, Zhengtao Yang, Shiwen Xu, Yongguo Cao, Naisheng Zhang

Affiliation

¹ Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, 130062, Jilin, People's Republic of China.

PMID: 24202549
DOI: 10.1007/s10753-013-9761-5

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.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Anti-Inflammatory Agents / pharmacology*
Cells, Cultured
Cyclooxygenase 2 / genetics
Cyclooxygenase 2 / metabolism
Dose-Response Relationship, Drug
Enzyme Activation
Female
Gene Expression Regulation / drug effects
I-kappa B Proteins / metabolism
Inflammation Mediators / metabolism*
Lipopolysaccharides / pharmacology*
Mammary Glands, Animal / drug effects*
Mammary Glands, Animal / enzymology
Mammary Glands, Animal / immunology
Mastitis / enzymology
Mastitis / genetics
Mastitis / immunology
Mastitis / prevention & control*
Mice
Mitogen-Activated Protein Kinases / metabolism*
NF-kappa B / metabolism*
Phosphorylation
Pregnancy
Primary Cell Culture
Signal Transduction / drug effects*
Sodium Selenite / pharmacology*
Tumor Necrosis Factor-alpha / genetics
Tumor Necrosis Factor-alpha / metabolism

Substances

Anti-Inflammatory Agents
I-kappa B Proteins
Inflammation Mediators
Lipopolysaccharides
NF-kappa B
Tumor Necrosis Factor-alpha
Ptgs2 protein, mouse
Cyclooxygenase 2
Mitogen-Activated Protein Kinases
Sodium Selenite