提高奶牛的抗氧化功能是增强免疫应答、降低乳房炎等炎性疾病发生的重要措施。核因子-κB (NF-κB)是一个对氧化还原反应敏感的转录因子和抗氧化作用的新靶点。项目将产奶性能、体细胞数、免疫指标、NF-κB信号通路、抗氧化酶、下游细胞因子的释放与NO的生成相结合，利用体内法研究了壳聚糖对泌乳前期高产奶牛抗氧化功能的影响及其机理。以奶牛外周血单个核细胞(PMBC)为模型，研究了壳聚糖对二乙烯三胺/一氧化氮聚合物或脂多糖诱导的细胞氧化损伤的保护作用；以诱导损伤的PMBC为模型，通过对NF-κB信号通路进行阻断和siRNA沉默基因NF-κBp65，研究了壳聚糖对NF-κB信号通路的转录活性、抗氧化酶、下游相关细胞因子的基因与蛋白质的表达及NO生成的调节作用，以及NF-κB信号通路的活性对IL-1和NO生成相关基因的调节作用，从NF-κB-IL-NO途径探讨了壳聚糖对奶牛抗氧化功能的调节机理。

Regulating and increasing antioxidative function was an important measure to ebhance immune response and reduce mastitis incidence of early lactating cows. The nuclear factor nuclear factor-kappa B (NF-κB) is a redox-sensitive transcription factor that is new target of antioxidative effect. The program was conducted to elucidate the mechanism on chitosan regulating antioxidative function of milking cow in early lactation by using feeding trial according to milk performane, somatic cell count, immune parameter, the activity and their gene and protein expression in NF-κB signaling pathway, anti-oxidative enzyme, related downstream cytokines as well as NO production. The regulation of chitosan on oxidative injury induced by diethylene triamine-nitric oxide Polymer or lipopolysaccharide in peripheral blood mononuclear cell (PMBC) was discussed. Oxidative stress-induced PMBC was served as a model to discuss the regulation of chitosan on the transcription activity of NF-κB signaling pathway, gene expression including antioxidative enzyme，related cytokines and NO production via blocking NF-κB signaling pathway and siRNA-mediated NF-κBp65 gene silencing, discussing the mechanism for chitosan to regulate oxidative function of dairy cows via NF-κB-NO pathway.