调节和提高奶牛乳腺上皮细胞（BMEC）中硫氧还蛋白还原酶（TrxR）的合成是减少乳腺氧化损伤的重要措施之一。以BMEC为模型，二乙烯三胺/一氧化氮聚合物为外源性NO供体，探讨硒对NO诱导的细胞损伤的保护作用及其对TrxR的调节作用。以2,4-二硝基氯苯（DNCB）抑制TrxR活性，探讨硒对NO生成的调节机理，及TrxR对白细胞介素类（IL）细胞因子的调节作用。以IL-1Ra为IL-1受体拮抗剂，或以相应的抑制剂阻断丝裂原激活蛋白激酶（MAPKs）信号通路，研究硒对TrxR活性、IL浓度、诱导型一氧化氮合酶和细胞凋亡信号激酶-1活性、MAPKs信号通路相关激酶磷酸化水平及其基因和蛋白质表达，以及NO 浓度的影响，从TrxR-IL-NO、TrxR-MAKPs-NO途径阐明硒对BMEC氧化应激损伤的保护作用。进一步通过siRNA沉默TrxR基因阐明硒通过TrxR缓解BMEC氧化应激损伤的机理。

Regulating and increasing the synthesis of thioredoxin reductase (TrxR) was an important measure to reduce oxidative injury of mammary gland of dairy cows. The program was conducted to elucidate the protective effects of selenium(Se) on oxidative injury induced by Diethylene Triamine-Nitric Oxide Polymer in bovine mammary epithelial cells(BMEC), and to discuss the regulation of Se on TrxR using in vitro experiment, and to determine the effects of Se on the NO production and the regulation of reducing TrxR activity on cytokine Interleukin(IL) production by using 2,4-dinitrochlorobenzene (DNCB) as inhibitor of TrxR. The activities and expressions of TrxR and inductible nitric oxide synthase by using DNCB as inhibitor of TrxR to induce the production of IL; or using IL-1Ra as antagonist of IL-1 receptor,or using relevant inhibitors to block mitogen-activated　protein　kinases (MAPKs) signal path and to discuss the mechanism for Se to attenuate oxidative injury of BMEC via TrxR-IL-NO pathway and TrxR-MAPKs-NO pathway modulated by TrxR according to phosphorylated　kinases related to MAPKs signal path and related gene expressions, contents and gene expressions of the related cytokine, inductible nitric oxide synthase. The study was further conducted to evaluate the mechanism for Se to attenuate BMEC oxidative injury via TrxR by siRNA-mediated TrxR gene silencing.