Myricetin relieves LPS-induced mastitis by inhibiting inflammatory response and repairing the blood-milk barrier
Myricetin relieves LPS-induced mastitis by inhibiting inflammatory response and repairing the blood-milk barrier
复制标题
杨梅素通过抑制炎症反应和修复血乳屏障缓解脂多糖引起的乳腺炎
DOI：
10.1002/jcp.28288
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发表时间：
2019-09-01
影响因子：
5.6
通讯作者：
Liu, Juxiong
中科院分区：
文献类型：
--
作者：
Kan, Xingchi;Liu, Bingrun;Liu, Juxiong
乳房炎是一种乳腺炎症，是一种严重影响世界各地奶牛健康的疾病。杨梅素是杨梅中的一种黄酮类化合物，具有抑制多种炎症反应的作用。本研究旨在评价杨梅素对内毒素(LPS)诱导的体内外乳房炎模型的影响，并阐明其作用机制。在体内实验中，杨梅素减轻炎性病变和中性粒细胞浸润的严重程度。此外，杨梅素可显著降低脂多糖诱导的髓过氧化物酶活性和肿瘤坏死因子-1、白介素6、白介素1的产生。杨梅素可增加乳房炎小鼠血乳屏障的完整性，上调紧密连接蛋白的表达。在体外，杨梅素可抑制脂多糖诱导的小鼠乳腺上皮细胞的炎症反应。在进一步的机制研究中，我们发现杨梅素的抗炎作用是通过在体内和体外抑制脂多糖诱导的AKT、IKK-、IB-和P65的磷酸化来实现的。综上所述，这些数据表明，杨梅素通过抑制AKT/IKK/NF-B信号通路和修复脂多糖诱导的小鼠乳房炎血乳屏障的完整性，有效地改善了炎症反应。
Mastitis, an inflammation of mammary gland, is a serious disease that affects the health of dairy cows around the world. Myricetin, a flavonoid from Bayberry, has been reported to suppress various inflammatory response. The aim of this study was to evaluate the effect of myricetin on lipopolysaccharide (LPS)-induced in vivo and in vitro mastitis model and clarify the underlying mechanism. In vivo experiments, myricetin attenuated the severity of inflammatory lesion and neutrophil infiltration. Moreover, myricetin pretreatment induced a significant decrease in the activity of myeloperoxidase (MPO) and the production of TNF-, IL-6, and IL-1 triggered by LPS. Myricetin pretreatment could also increase the integrity of the blood-milk barrier and upregulate the tight junction proteins in LPS-induced mice mastitis. In vitro, myricetin inhibited LPS-induced inflammatory response in mice mammary epithelial cells (mMECs). In the further mechanism studies, we found that the anti-inflammatory effect of myricetin was mediated by inhibiting LPS-induced phosphorylation of AKT, IKK-, IB-, and P65 in vivo and in vitro. Collectively, these data suggested that myricetin effectively ameliorated the inflammatory response by inhibiting the AKT/IKK/NF-B signaling pathway and repairing the integrity of blood-milk barrier in LPS-induced mice mastitis.