Ethanol Extract of Artemisia Annua Prevents LPS-Induced Inflammation and Blood-Milk Barrier Disruption in Bovine Mammary Epithelial Cells

文献类型： 外文期刊

第一作者： Song, Jie

作者： Song, Jie;Hu, Yao;Ao, Changjin;Wang, Lifang

作者机构：

关键词： Artemisia annua extract; lipopolysaccharide; inflammation; CD36; tight junction proteins

期刊名称：ANIMALS （ 影响因子：3.231； 五年影响因子：3.312 ）

ISSN： 2076-2615

年卷期： 2022 年 12 卷 10 期

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收录情况： SCI

摘要： Simple Summary Mastitis is one of the most serious diseases restricting the development of the dairy industry. It not only affects bovine production performance, but also leads to antibiotic residues and drug resistance. As antibiotics have gradually been forbidden, it is urgently necessary to find natural alternatives to prevent mastitis. Artemisia annua is an annual low-toxicity herb native to China that is widely distributed around the world. This study aimed to explore whether an ethanol extract of Artemisia annua (AAE) could be used as a new preventive agent to ameliorate LPS-induced inflammation and blood-milk barrier disruption in bovine mammary epithelial cells (bMECs). Our results showed that AAE pretreatment could alleviate inflammatory injury and tight junction abnormalities after LPS challenge, which was partially related to the attenuation of nuclear factor-kappa B (NF-kappa B) signaling and the downregulation of CD36 levels. Our study can provide a certain reference value for the development and utilization of plant extracts. This experiment evaluated the pre-protective effect of AAE on inflammatory injury and tight junction disturbance in bMECs induced by LPS. The bMECs were treated with AAE (3, 6, 12 mu g/mL) for 3 h and then incubated with 10 mu g/mL lipopolysaccharide (LPS) for 12 h. Our results showed that LPS significantly increased the mRNA and protein expression of CD36, induced the phosphorylation of I kappa B alpha and p65 and elevated the levels of TNF-alpha, IL-1 beta and IL-6 mRNA, which further resulted in ultrastructural damage, disrupted the expression of tight junction proteins (occludin, zonula occludens (ZO-1) and claudin-1) and decreased the viability of bMECs (p < 0.05). More importantly, AAE pretreatment attenuated the expression of CD36, suppressed the activity of the NF-kappa B signaling pathway and down-regulated the levels of inflammatory factors in LPS-stimulated bMECs (p < 0.05). Therefore, AAE can effectively protect bMECs against inflammatory injury and tight junction dysfunction, which has important research value for the prevention of bovine mastitis.

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