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香草醛可保护血乳屏障并抑制 LPS 诱导的乳腺炎中炎症反应。

Vanillin protects the blood-milk barrier and inhibits the inflammatory response in LPS-induced mastitis in mice.

机构信息

College of Veterinary Medicine, Jilin University, Changchun 130062, China.

Laboratory of Biomolecular Research, Division of Biology and Chemistry, Paul Scherrer Institute, Villigen CH-5232, Switzerland.

出版信息

Toxicol Appl Pharmacol. 2019 Feb 15;365:9-18. doi: 10.1016/j.taap.2018.12.022. Epub 2019 Jan 2.

DOI:10.1016/j.taap.2018.12.022
PMID:30610879
Abstract

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.

摘要

香草醛在食品、化学和制药等多种领域均有应用,具有抗炎特性。然而,目前尚无关于香草醛对脂多糖(LPS)诱导乳腺炎影响的报道。本研究旨在探讨香草醛对 LPS 诱导乳腺炎后续炎症反应和血乳屏障的影响。结果表明,香草醛通过以下方式抑制炎症反应:a)抑制髓过氧化物酶活性;b)减少促炎介质的产生,包括肿瘤坏死因子-α(Tnf-α;从 128.5±14.59 降至 67.51±10.88,pg/mL,P<0.01)、白细胞介素-6(Il-6;从 531.5±196.4 降至 109.3±24.14,pg/mL,P<0.05)、白细胞介素-1β(Il-1β;从 2569±1648 降至 731.8±171.7,pg/mL,P<0.05)、诱导型一氧化氮合酶(Inos)和环氧化酶-2(Cox-2);c)通过增加紧密连接蛋白的蛋白水平来修复血乳屏障,包括紧密连接蛋白 1(Zo-1)、claudin-3 和闭合蛋白。在体外实验中,香草醛可以抑制 LPS 诱导的炎症反应,并增强紧密连接蛋白的蛋白水平。进一步的研究表明,香草醛通过抑制丝裂原活化蛋白激酶(MAPKs)和核因子 kappa-轻链增强子的 B 细胞(NF-κB)信号通路来抑制炎症反应。本研究结果表明,香草醛通过增强血乳屏障和抑制炎症反应来保护乳腺免受 LPS 诱导的乳腺炎的侵害。

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