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