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[Objectives] This paper is based on the previous study on the breast-protecting function of the renin-angiotensin system (RAS).Here we further studied one of the main members in this family, angiotensin converting enzyme2 (ACE2), on its function and mechanism in AngII induced oxidative stress, inflammation injury and apoptosis. [Methods] The Holstein cows with 6 healthy lactation periods were randomly divided into the control groupm (cencontrate):m (forage)=4:6and the high grain diet groupm (cencontrate):m (forage)=6:4, and the single column fixed time quantitative feeding was used. After feeding for 20 weeks, the breast tissue was taken from the living body. The following experiments were carried out:1) determine the oxidative stress index of·OH, TNOS and SOD in mammary tissue; 2) ELISA method was used to determine TNF-α, IL-1β inflammatory index and Caspase-3, Bax, Bcl-2 apoptosis index; 3) Western blot analyzed the expression of ACE2 and ACE protein in breast tissue. [Results] Comparing with control group, the level of·OH in the mammary gland tissues of dairy cows fed the high grain diet increased significantly (P < 0.01), the activity of TNOS and SOD decreased, and the activity of TNOS decreased significantly (P < 0.05), the levels of TNF-α and IL-1β of inflammatory factors increased significantly (P < 0.05), and Caspase-3 and Bax levels of apoptotic protein increased significantly (P < 0.01). The level of inhibition of apoptotic protein Bcl-2 significantly decreased (P < 0.05);the concentration of AngII and the expression of ACE protein in breast tissue increased significantly (P < 0.05), and the concentration of Ang1-7 and the expression of ACE2 protein decreased significantly (P < 0.05). [Conclusions] Long-term feeding of high grain diet can cause a certain degree of damage to the mammary gland tissue of dairy cows and cause recessive mastitis, which shows a significant increase in the release of·OH, the decrease of antioxidant enzyme activity, and the enhancement of the inflammatory response to the apoptosis of the cells. In this process, the local RAS system of the breast was activated, the key members of the ACE-AngII-AT1R axis, ACE and AngII, were significantly increased, and the key members of the ACE2-Ang1-7-MasR axis ACE2 and Ang1-7 were significantly reduced. The results suggest that the imbalance of the two axis of the RAS system in the local mammary gland, with lower level of ACE2 and the high level of AngII, may be the main mechanism of breast injury. [ABSTRACT FROM AUTHOR]