The Protective Effect of Selenium on Bovine Mammary Epithelial Cell Injury Caused by Depression of Thioredoxin Reductase
The Protective Effect of Selenium on Bovine Mammary Epithelial Cell Injury Caused by Depression of Thioredoxin Reductase
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硒对硫氧还蛋白还原酶抑制所致牛乳腺上皮细胞损伤的保护作用
DOI：
10.1007/s12011-017-1175-z
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发表时间：
2018-07-01
影响因子：
3.9
通讯作者：
Shi, Binlin
中科院分区：
文献类型：
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作者：
Guo, Yongmei;Yan, Sumei;Shi, Binlin
为了阐明硒（Se）对奶牛乳腺抗氧化功能的影响及其潜在机制，采用单因素完全随机设计研究进行了实验。牛乳腺上皮细胞（BMEC）被随机分为四组：对照组、硒处理组、2,4-二硝基氯苯（DNCB）抑制组和硒预防组。研究发现，用 Se 处理 BMEC 可以显着逆转 DNCB 暴露后细胞增殖和硫氧还蛋白还原酶 (TrxR) 表达的下降。在用 Se 处理的 BMEC 中，DNCB 诱导的细胞凋亡信号激酶 1 (ASK-1) 激活减少，该激酶激活丝裂原激活蛋白激酶 (MAPK) 途径。此外，我们的结果表明，硒处理导致细胞内花生四烯酸（ARA）和15-氢过氧二十碳四烯酸（15-HPETE）的积累降低，这是由于在DNCB刺激的BMEC中受p38MAPK和c-Jun N末端激酶（JNK）调节的胞质磷脂酶A2（cPLA2）的表达受到抑制。综上所述，硒处理主要通过增加TrxR的活性，抑制MAPK信号通路的激活，从而降低ARA及其相关代谢物的含量，改善奶牛乳腺的抗氧化功能，保护细胞免受氧化损伤。
To elucidate the effect of selenium (Se) on antioxidant function of mammary glands in dairy cows and the underlying mechanism, an experiment was conducted using a single-factor completely randomized design study. Bovine mammary epithelial cells (BMECs) were randomly divided into four groups: control, Se treatment, 2,4-dinitrochlorobenzene (DNCB) inhibition, and Se prevention. Treatment of BMECs with Se was found to significantly reverse decreased cell proliferation and the expression of thioredoxin reductase (TrxR) after DNCB exposure. DNCB-induced activation of apoptosis signaling kinase-1 (ASK-1), which activates the mitogen-activated protein kinase (MAPK) pathway, was reduced in BMECs treated with Se. Additionally, our results indicated that Se treatment resulted in lower intracellular accumulation of arachidonic acid (ARA) and 15-hydroperoxyeicosatetraenoic acid (15-HPETE) due to suppressed expression of cytosolic phospholipase A2(cPLA2) regulated by p38MAPK and c-Jun N-terminal kinase (JNK) in DNCB-stimulated BMECs. Taken together, these findings suggest that Se treatment improved the antioxidant function of dairy cow mammary glands and protected cells from oxidative damage primarily by increasing the activity of TrxR, inhibiting the activation of the MAPK signaling pathway, and thus decreasing the content of ARA and its related metabolites.