College of Animal Science, Inner Mongolia Agricultural University, Hohhot, 010018, China.
Biol Trace Elem Res. 2018 Jul;184(1):75-82. doi: 10.1007/s12011-017-1175-z. Epub 2017 Oct 11.
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 A (cPLA) 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.
为了阐明硒（Se）对奶牛乳腺抗氧化功能的影响及其机制，本实验采用单因素完全随机设计研究。将奶牛乳腺上皮细胞（BMECs）随机分为四组：对照组、Se 处理组、2,4-二硝基氯苯（DNCB）抑制组和 Se 预防组。结果发现，Se 处理可显著逆转 DNCB 暴露后细胞增殖和硫氧还蛋白还原酶（TrxR）表达的降低。DNCB 诱导的凋亡信号激酶-1（ASK-1）激活，进而激活丝裂原活化蛋白激酶（MAPK）途径，在 Se 处理的 BMECs 中减少。此外，我们的结果表明，由于 p38MAPK 和 c-Jun N-末端激酶（JNK）调节的胞质型磷脂酶 A（cPLA）表达下调，DNCB 刺激的 BMECs 中 ARA 和 15-羟过氧二十碳四烯酸（15-HPETE）的细胞内积累减少，导致 Se 处理。综上所述，这些发现表明，Se 处理可改善奶牛乳腺的抗氧化功能，保护细胞免受氧化损伤，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。
