BACKGROUND & AIMS:
:Mastitis is one of three bovine diseases recognized as a cause of substantial economic losses every year throughout the world. Niacin is an important feed additive that is used extensively for dairy cow nutrition. However, the mechanism by which niacin acts on mastitis is not clear. The aim of this study is to investigate the mechanism of niacin in alleviating the inflammatory response of mammary epithelial cells and in anti-mastitis. Mammary glands, milk, and blood samples were collected from mastitis cows not treated with niacin (n = 3) and treated with niacin (30 g/d, n = 3) and healthy cows (n = 3). The expression of GPR109A, IL-6, IL-1β, and TNF-α in the mammary glands of the dairy cows with mastitis was significantly higher than it was in the glands of the healthy dairy cows. We also conducted animal experiments in vivo by feeding rumen-bypassed niacin. Compared with those in the untreated mastitis group, the somatic cell counts (SCCs) and the expression of IL-6, IL-1β, and TNF-α in the blood and milk were lower. In vitro, we isolated the primary bovine mammary epithelial cells (BMECs) from the mammary glands of the healthy cows. The mRNA levels of IL-6, IL-1β, TNF-α, and autophagy-related genes were detected after adding niacin, shRNA, compound C, trans retinoic acid, 3-methyladenine to BMECs. Then GPR109A, AMPK, NRF-2, and autophagy-related proteins were detected by Western blot. We found that niacin can activate GPR109A and phosphorylate AMPK, and promote NRF-2 nuclear import and autophagy to alleviate LPS-induced inflammatory response in BMECs. In summary, we found that niacin can reduce the inflammatory response of BMECs through GPR109A/AMPK/NRF-2/autophagy. We also preliminarily explored the alleviative effect of niacin on mastitis in dairy cows.
背景与目标:
:乳腺炎是被公认为全世界每年造成重大经济损失的三种牛病之一。烟酸是一种重要的饲料添加剂,已广泛用于奶牛营养。但是,烟酸对乳腺炎起作用的机制尚不清楚。这项研究的目的是研究烟酸减轻乳腺上皮细胞和抗乳腺炎的炎症反应的机制。从未使用烟酸(n = 3),未使用烟酸(30 g / d,n = 3)和健康的母牛(n = 3)处理的乳腺炎奶牛中收集乳腺,牛奶和血液样本。 GPR109A,IL-6,IL-1β和TNF-α在患有乳腺炎的奶牛的乳腺中的表达明显高于在健康奶牛的乳腺中的表达。我们还通过饲喂瘤胃绕过的烟酸进行了体内动物实验。与未治疗的乳腺炎组相比,血液和牛奶中的体细胞计数(SCC)以及IL-6,IL-1β和TNF-α的表达较低。在体外,我们从健康母牛的乳腺中分离出了原代的牛乳腺上皮细胞(BMEC)。向BMECs中添加烟酸,shRNA,化合物C,反式维甲酸,3-甲基腺嘌呤后,检测IL-6,IL-1β,TNF-α和自噬相关基因的mRNA水平。然后通过蛋白质印迹检测GPR109A,AMPK,NRF-2和自噬相关蛋白。我们发现烟酸可以激活GPR109A并磷酸化AMPK,并促进NRF-2核的导入和自噬,从而减轻LPEC诱导的BMEC炎症反应。总之,我们发现烟酸可以通过GPR109A / AMPK / NRF-2 /自噬减少BMEC的炎症反应。我们还初步探讨了烟酸对奶牛乳腺炎的缓解作用。