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甘草查尔酮 A 可保护血乳屏障完整性并缓解 LPS 诱导的乳腺炎中的炎症反应。

Licochalcone A Protects the Blood-Milk Barrier Integrity and Relieves the Inflammatory Response in LPS-Induced Mastitis.

机构信息

College of Animal Science and Veterinary Medicine, Jilin University, Changchun, China.

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

出版信息

Front Immunol. 2019 Feb 25;10:287. doi: 10.3389/fimmu.2019.00287. eCollection 2019.

Abstract

Mastitis is an acute clinical inflammatory response. The occurrence and development of mastitis seriously disturb women's physical and mental health. Licochalcone A, a phenolic compound in , has anti-inflammatory properties. Here, we examined the effect of licochalcone A on blood-milk barrier and inflammatory response in LPS-induced mice mastitis. , we firstly established mice models of mastitis by canal injection of LPS to mammary gland, and then detected the effect of licochalcone A on pathological indexes, inflammatory responses and blood-milk barrier in this model. , Mouse mammary epithelial cells (mMECs) were treated with licochalcone A prior to the incubation of LPS, and then the inflammatory responses, tight junction which is the basic structure of blood-milk barrier were analyzed. Last, we elucidated the anti-inflammatory mechanism by examining the activation of mitogen-activated protein kinase MAPK) and AKT/NF-κB signaling pathways and . The results showed that licochalcone A significantly decreased the histopathological impairment and the inflammatory responses, and improved integrity of blood-milk barrier. The results demonstrated that licochalcone A inhibited LPS-induced inflammatory responses and increase the protein levels of ZO-1, occludin, and claudin3 in mMECs. The and mechanistic study found that the anti-inflammatory effect of licochalcone A in LPS-induced mice mastitis was mediated by MAPK and AKT/NF-κB signaling pathways. Our experiments collectively indicate that licochalcone A protected against LPS-induced mice mastitis via improving the blood-milk barrier integrity and inhibits the inflammatory response by MAPK and AKT/NF-κB signaling pathways.

摘要

乳腺炎是一种急性临床炎症反应。乳腺炎的发生和发展严重扰乱了妇女的身心健康。甘草查尔酮 A 是一种酚类化合物,具有抗炎作用。在这里,我们研究了甘草查尔酮 A 对 LPS 诱导的小鼠乳腺炎血乳屏障和炎症反应的影响。首先,我们通过向乳腺管内注射 LPS 建立了乳腺炎小鼠模型,然后检测了甘草查尔酮 A 对该模型中病理指标、炎症反应和血乳屏障的影响。接下来,我们在 LPS 孵育前用甘草查尔酮 A 处理小鼠乳腺上皮细胞(mMECs),然后分析炎症反应和血乳屏障的基本结构紧密连接。最后,通过检测丝裂原活化蛋白激酶(MAPK)和 AKT/NF-κB 信号通路的激活,阐明了抗炎机制。结果表明,甘草查尔酮 A 显著降低了组织病理学损伤和炎症反应,改善了血乳屏障的完整性。结果表明,甘草查尔酮 A 抑制了 LPS 诱导的炎症反应,并增加了 mMECs 中 ZO-1、occludin 和 claudin3 的蛋白水平。机制研究表明,甘草查尔酮 A 通过 MAPK 和 AKT/NF-κB 信号通路介导 LPS 诱导的乳腺炎小鼠的抗炎作用。我们的实验表明,甘草查尔酮 A 通过改善血乳屏障的完整性来保护 LPS 诱导的乳腺炎小鼠,并通过 MAPK 和 AKT/NF-κB 信号通路抑制炎症反应。

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