Abstract

Omega-3 polyunsaturated fatty acids (n-3 PUFAs), essential fatty acids for humans and animals, have been reported to play a beneficial role in a variety of inflammatory diseases. In this study, we investigated the inhibitory effects and potential molecular mechanisms of n-3 PUFAs on the inflammatory response in lipopolysaccharide (LPS)-stimulated mammary alveolar cell line (MAC-T). Results showed that n-3 PUFAs could abate LPS-induced secretions of tumor necrosis factor-α, interleukin (IL)-6 and IL-1β in MAC-T cells through the nuclear transcription factor kappa B (NF-κB) signal pathway. Meanwhile, n-3 PUFA intervention attenuated histopathologic changes of mammary glands, the white blood cell number decrease, and the alkaline phosphatase level decrease in the serum of mice challenged by LPS. Furthermore, n-3 PUFA intervention improved the ecological structure of the flora in terms of the structural disorder of the non-significant dominant flora induced by LPS in mice. Collectively, both in vitro and in vivo experiments revealed that n-3 PUFAs have a positive effect on LPS-induced inflammatory response, which was possibly mediated by the NF-κB signaling pathway and the intestinal microbiota.

中文翻译：

---

Omega-3多不饱和脂肪酸改善脂多糖诱导的乳腺上皮细胞和乳腺炎症反应

摘要

据报道，Omega-3 多不饱和脂肪酸 (n-3 PUFA) 是人类和动物的必需脂肪酸，在多种炎症性疾病中发挥有益作用。在这项研究中，我们研究了 n-3 PUFAs 对脂多糖 (LPS) 刺激的乳腺肺泡细胞系 (MAC-T) 炎症反应的抑制作用和潜在的分子机制。结果表明，n-3 PUFAs可以通过核转录因子κB（NF-κB）信号通路减少LPS诱导的MAC-T细胞中肿瘤坏死因子-α、白细胞介素（IL）-6和IL-1β的分泌。同时，n-3 PUFA干预减轻了LPS攻击小鼠的乳腺组织病理学变化，白细胞数量减少，碱性磷酸酶水平降低。此外，n-3 PUFA 干预改善了植物群的生态结构，改善了由 LPS 诱导的小鼠非显着优势菌群的结构紊乱。两者共同体外和体内实验表明，n-3 PUFAs 对 LPS 诱导的炎症反应具有积极作用，这可能是由 NF-κB 信号通路和肠道微生物群介导的。