Selenium Inhibits LPS-Induced Pro-inflammatory Gene Expression by Modulating MAPK and NF-κB Signaling Pathways in Mouse Mammary Epithelial Cells in Primary Culture
Selenium Inhibits LPS-Induced Pro-inflammatory Gene Expression by Modulating MAPK and NF-κB Signaling Pathways in Mouse Mammary Epithelial Cells in Primary Culture
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DOI：
10.1007/s10753-013-9761-5
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发表时间：
2014-04-01
期刊：
影响因子：
5.1
通讯作者：
Zhang, Naisheng
中科院分区：
文献类型：
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作者：
Zhang, Wen;Zhang, Runxiang;Zhang, Naisheng
乳腺炎的特点是哺乳动物和人类乳腺的炎症；这种情况是造成乳制品行业经济损失的主要原因之一。硒（Se）是一种生物微量元素，可以调节信号转导中许多调节蛋白的功能，并为患有炎症性疾病（包括乳腺炎）的动物提供益处。本研究旨在探讨Na2SeO3对脂多糖（LPS）诱导的小鼠乳腺上皮细胞（MMECs）炎症的保护作用及其作用机制。我们的研究结果表明，在硒缺乏的mmec中补充硒后，lps诱导的环氧化酶-2和肿瘤坏死因子- α的表达显著降低。Na2SeO3还以剂量依赖性的方式抑制lps诱导的核因子κ B活化，抑制κ B降解，以及ERK， JNK和P38磷酸化。提示硒在乳腺炎中具有抗炎作用。
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 Na2SeO3 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-alpha significantly decreased after Se was supplemented to Se-deficient MMECs. Na2SeO3 also suppressed LPS-induced nuclear factor-kappa B 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.