Mechanism Underlying the Protective Effect of Selenium on NO-Induced Oxidative Damage in Bovine Mammary Epithelial Cells
Mechanism Underlying the Protective Effect of Selenium on NO-Induced Oxidative Damage in Bovine Mammary Epithelial Cells
复制标题
硒对 NO 诱导的牛乳腺上皮细胞氧化损伤保护作用的机制
DOI：
10.1007/s12011-018-1603-8
复制
发表时间：
2019-01
影响因子：
3.9
通讯作者：
Shi Binlin
中科院分区：
文献类型：
--
作者：
Guo Yongmei;Guo Xiaoyu;Yan Sumei;Zhang Boqi;Shi Binlin
本试验旨在探讨硒对一氧化氮（NO）损伤的牛乳腺上皮细胞（BMEC）抗氧化和免疫功能的影响及其机制。将第三代BMEC随机分为8个处理，每个处理6个重复。对照组在不含硒和二乙烯三胺/NO（DETA/NO）的培养基中培养30 h。DETA/NO组和Se保护组分别暴露于不同浓度的Se（0、10、20、50、100、150和200 nmol/L）24 h后，再用DETA/NO（1000 μmol/L）处理6 h。与对照组相比，DETA/NO组细胞增殖率和硫氧还蛋白还原酶活性（TrxR;P< 0.05）降低。此外，DETA/NO还可降低核因子E2相关因子2（Nrf 2）和TrxR的基因表达，以及TrxR的蛋白表达水平。诱导型一氧化氮合酶（iNOS）活性、表达水平、白细胞介素1β（IL 1β）浓度、基因表达水平和NO浓度均显著升高（P< 0.05）。丝裂原活化蛋白激酶（MAPK）信号通路相关指标的基因表达水平也有类似的变化。硒处理BMEC可显著逆转DETA/NO引起的变化，并呈线性或二次剂量依赖性（P< 0.05），50 nmol/L时效果最好。这些数据表明，硒提高BMEC的抗氧化功能，并保护细胞免受DETA/NO诱导的氧化损伤，主要是通过提高TrxR的活性和降低NO的浓度，通过调节Nrf 2和MAPK信号通路。
This experiment was conducted to investigate the effects and mechanism of selenium (Se) on antioxidant and immune function of bovine mammary epithelial cells (BMEC) damaged by nitric oxide (NO). The third-generation BMEC was randomly divided into eight treatments with six replicates. The BMEC in the control group was cultured in the medium without Se and diethylenetriamine/NO (DETA/NO) for 30 h. For the DETA/NO group and Se protection group BMEC were exposed to different concentrations of Se (0, 10, 20, 50, 100, 150, and 200 nmol/L) for 24 h, followed by treatment with DETA/NO (1000 μmol/L) for 6 h. Compared with the control group, DETA/NO decreased proliferation rate and activity of thioredoxin reductase (TrxR;P< 0.05). Additionally, DETA/NO decreased the gene expression of both nuclear factor-E2-related factor 2 (Nrf2) and TrxR, as well as the protein expression level of TrxR. However, the activity, and expression levels of inducible nitric oxide synthase (iNOS), as well as the concentration and gene expression level of interleukin-1β (IL-1β) and the concentration of NO significantly increased (P< 0.05). The gene expression levels of indexes related to the mitogen-activated protein kinase (MAPK) signaling pathway showed similar changes. Treatment of BMEC with Se significantly reversed DETA/NO-induced changes in a linear or quadratic dose-dependent manner (P< 0.05), with greatest benefit at 50 nmol/L. These data suggests that Se improves the antioxidant function of BMEC, and protects cells from DETA/NO-induced oxidative damage, primarily by enhancing the activity of TrxR and decreasing the concentration of NO through modulation of Nrf2 and MAPK signaling pathways.
登录
查看更多内容
影响因子：
3.9
作者：
Yachao Wang;Li Jiang;Yuanfeng Li;Xuegang Luo;Jian He
通讯作者：
Yachao Wang;Li Jiang;Yuanfeng Li;Xuegang Luo;Jian He
影响因子：
6.6
作者：
A. A. Mongin-A.;Preeti Dohare;D. Jourd’heuil
通讯作者：
A. A. Mongin-A.;Preeti Dohare;D. Jourd’heuil
影响因子：
6.6
作者：
Mo, Chunfen;Wang, Ling;Xiao, Hengyi
通讯作者：
Xiao, Hengyi
影响因子：
6
作者：
J. Wissel;P. Kaňovský;E. Růžička;Martin Bareš;H. Hortová;H. Streitová;R. Jech;Jan Roth;
通讯作者：
J. Wissel;P. Kaňovský;E. Růžička;Martin Bareš;H. Hortová;H. Streitová;R. Jech;Jan Roth;
影响因子：
4.2
作者：
Schrauzer, GN
通讯作者：
Schrauzer, GN