断奶仔猪生产过程所遭遇的氧化应激，是导致肠道功能损伤的主要诱因，已成为制约集约化养猪可持续发展的瓶颈。天冬氨酸是仔猪肠黏膜主要能量来源之一，处于机体代谢网络的独特位置，具有调控机体氧化还原状态的功能，然而其对肠上皮细胞线粒体氧化应激反应的作用及分子机制尚不清楚。本项目通过构建仔猪氧化应激和猪肠上皮细胞氧化损伤模型，探讨天冬氨酸对仔猪肠上皮细胞氧化-抗氧化水平（氧自由基和谷胱甘肽含量、标志基因HSP70和HSP60表达）、线粒体功能（线粒体数量和形态、线粒体呼吸代谢、膜电位变化）以及RIPK1信号通路的影响，并利用特异性抑制剂和激动剂靶向调控猪肠上皮细胞RIPK1活性，从而进一步揭示天冬氨酸对RIPK1信号通路介导的猪肠上皮细胞氧化应激的干预机制。本项目将为缓解仔猪肠道氧化损伤、控制仔猪氧化应激提供营养调控手段，为进一步丰富仔猪肠道氧化应激氨基酸综合调控理论提供基础。

Oxidative stress is the main inducement of intestinal function injury during the production process of weaned piglets，which has become a bottleneck restricting in the sustainable development of intensive pig farming. Asparate, as one of the main energy sources in the intestinal mucosa of piglets, lies at a unique node of metabolic network and has function as regulating redox homeostasis. However, the effect mechanism of asparate on mitochondrial oxidative stress in intestinal epithelial cells has not well understood. This project aims to address the effects of asparate on the oxidation-antioxidant levels (oxygen free radical, glutathione level, the expression of marker genes HSP70 and HSP60), mitochondrial function (mitochondria number and morphology, mitochondrial respiration metabolism, membrane potential changes), as well as the RIPK1 signaling pathway, in experimental models of diquat-induced oxidative stress both in vivo using piglets and in vitro. Moreover, RIPK1 activity will be regulated by targeted inhibitor or activator, in order to further explore the interventional mechanism of asparate on RIPK1 signaling pathway in intestinal epithelial cell of piglets under oxidative stress. Our study will provide nutritional regulation means for the alleviation of intestinal injury and control of oxidative stress in piglets. It will also provide a basis for further enriching the comprehensive regulation theory of amino acids in intestinal piglets under oxidative stress.