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Mediators of Inflammation
Volume 2018, Article ID 4093285, 10 pages
Research Article

CYP1A1 Relieves Lipopolysaccharide-Induced Inflammatory Responses in Bovine Mammary Epithelial Cells

1College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi 712100, China
2Innovation Experimental College, Northwest A&F University, Yangling, Shaanxi 712100, China
3Key Laboratory of Animal Biotechnology, Ministry of Agriculture, Northwest A&F University, Yangling, Shaanxi 712100, China

Correspondence should be addressed to Yong Zhang; nc.ude.fauswn@6591gnoygnahz and Ming-Qing Gao; nc.ude.ufawn@gniqgnimoag

Received 30 July 2017; Revised 29 November 2017; Accepted 11 December 2017; Published 28 February 2018

Academic Editor: Anshu Agrawal

Copyright © 2018 Wen-Yao Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The expression of cytochrome P4501A1 (CYP1A1) enzyme is changed in various organs during the host response to inflammation or infection, leading to alterations in the metabolism of endogenous and exogenous compounds. Results of this study showed that CYP1A1 expression was significantly downregulated in the mammary tissue of bovine with mastitis, in inflammatory epithelial cells (INEs) extracted from the tissue, and in lipopolysaccharide- (LPS-) induced INEs compared with their corresponding counterparts. Overexpression of CYP1A1 in bovine mammary epithelial cells alleviated the LPS-induced inhibition of epithelial proliferation, abated the LPS-induced increase of gene expression and protein secretion of inflammatory cytokine tumor necrosis factor-α and interleukin-6, and attenuated the LPS-induced activation of NF-κB signaling. These findings suggest that CYP1A1 has immense potential in the regulation of inflammatory responses in bovine mammary epithelial cells during mastitis and may serve as a useful therapeutic target in mitigating injuries caused by inflammatory overreaction.