Vanillin is used in a variety of food, chemical, and pharmaceutical applications, and exhibits anti-inflammatory properties. However, there are no reports about the effects of vanillin on lipopolysaccharide (LPS)-induced mastitis. In this study, we explored the effects of vanillin on the subsequent inflammatory response and blood-milk barrier in LPS-induced mastitis. Results showed that vanillin suppressed the inflammatory response by a) inhibiting myeloperoxidase activity; b) decreasing the production of pro-inflammatory mediators which include tumor necrosis factor alpha (Tnf-α; from 128.5 ± 14.59 to 67.51 ± 10.88,pg/mL, P < 0.01), interleukin-6 (Il-6; from 531.5 ± 196.4 to 109.3 ± 24.14, pg/mL, P < 0.05), interleukin-1β (Il-1β; from 2569 ± 1648 to 731.8 ± 171.7, pg/mL, P < 0.05), inducible nitric oxide synthase (Inos), and cyclooxygenase-2 (Cox-2); and c) repairing the blood-milk barrier by increasing the protein levels of the tight junction proteins, including zona occludens 1 (Zo-1), claudin-3, and occludin. In vitro experiment, Vanillin can inhibit LPS-induced inflammation and enhance the protein levels of tight junction proteins. Further studies have shown that vanillin inhibits inflammation by inhibiting mitogen-activated protein kinases (MAPKs) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathways. Our findings showed that vanillin protects mammary gland from LPS-induced mastitis by enhancing the blood-milk barrier and inhibiting the inflammatory response.
Keywords: Blood–Milk Barrier; MAPK; Mastitis; NF-κB; Vanillin.
Copyright © 2018. Published by Elsevier Inc.