ACTA VETERINARIA ET ZOOTECHNICA SINICA ›› 2019, Vol. 50 ›› Issue (7): 1458-1465.doi: 10.11843/j.issn.0366-6964.2019.07.015

• BASIC VETERINARY MEDICINE • Previous Articles     Next Articles

Angiotensin-converting Enzyme 2 on Ang Ⅱ-induced Mitigation of Inflammatory Injury in Bovine Mammary Epithelial Cells

ZHU Bin, LIU Xiaoqian, LIU Ying, JI Xiaoxia, ZHANG Yuanshu*   

  1. Key Laboratory of Animal Physiology and Biochemistry of Ministry of Agriculture, Nanjing Agricultural University, Nanjing 210095, China
  • Received:2019-01-30 Online:2019-07-23 Published:2019-07-23

Abstract: Inflammatory damage of bovine mammary epithelial cells (MAC-T) was induced by different concentrations of angiotensin Ⅱ (Ang Ⅱ), and the changes of angiotensin-converting enzyme 2 (ACE 2) and the interaction with Ang Ⅱ were explored. The research includes:Detecting the secretion or release of inflammatory factors in cell supernatant by ELISA; Western blot analysis of protein expression changes of ACE 2 and ACE, and correlation analysis; The protective effect of ACE 2 active protein on Ang Ⅱ induced injury. Results were as follows:1) The levels of pro-inflammatory factors TNF-α, IL-6 and IL-8 in the supernatant of bovine MAC-T cells in the Ang Ⅱ treatment were significantly (P<0.05) or very significantly increased (P<0.01), the anti-inflammatory factor IL-10 content was significantly reduced (P<0.05); 2) Treatment with different concentrations of Ang Ⅱ, the expression of ACE 2 protein was decreased, and the 10-6 mol·L-1 Ang Ⅱ treatment group was significantly decreased (P<0.05); the expression of ACE protein was reversed. There was a significant negative correlation between ACE 2 and Ang Ⅱ concentrations; 3) After adding exogenous ACE 2 active protein, the results showed that the concentration of TNF-α, IL-6 and IL-8 in the supernatant of the cells decreased to some extent, and the concentration of IL-10 increased. The imbalance of the ACE 2/ACE axis is the main cause of inflammatory injury induced by Ang Ⅱ. The conclusion showed that high level of Ang Ⅱ can activate inflammatory factors to promote inflammatory response and is the main mediator of inflammatory response. ACE 2 can inhibit the up-regulation of inflammatory response by degrading Ang Ⅱ.

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