College of Veterinary Medicine, Yangzhou University, Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Disease and Zoonoses, Yangzhou, Jiangsu, PR China.
Joint International Research Laboratory of Agriculture and Agriproduct Safety of the Ministry of Education, Yangzhou, Jiangsu, PR China.
BMC Vet Res. 2024 Aug 27;20(1):383. doi: 10.1186/s12917-024-04240-3.
An elevated endogenous cortisol level due to the peripartum stress is one of the risk factors of postpartum bovine uterine infections. Selenium is a trace element that elicits anti-inflammation and antioxidation properties. This study aimed to reveal the modulatory effect of selenium on the inflammatory response of primary bovine endometrial stromal cells in the presence of high-level cortisol. The cells were subjected to lipopolysaccharide to establish cellular inflammation. The mRNA expression of toll-like receptor 4 (TLR4), proinflammatory factors, and selenoproteins was measured with qPCR. The activation of NF-κB and MAPK signalling pathways was detected with Western blot and immunofluorescence.
The pretreatment with sodium selenite (2 and 4 µΜ) resulted in a down-regulation of TLR4 and genes encoding proinflammatory factors, including interleukin (IL)-1β, IL-6, IL-8, tumour necrosis factor α, cyclooxygenase 2, and inducible nitric oxide synthase. Selenium inhibited the activation of NF-κB and the phosphorylation of mitogen-activated protein kinase kinase, extracellular signal-regulated kinase, p38MAPK and c-Jun N-terminal kinase/stress-activated protein kinase. The suppression of those genes and pathways by selenium was more significant in the presence of high cortisol level (30 ng/mL). Meanwhile the gene expression of glutathione peroxidase 1 and 4 was promoted by selenium, and was even higher in the presence of cortisol and selenium.
The anti-inflammatory action of selenium is probably mediated through NF-κB and MAPK, and is augmented by cortisol in primary bovine endometrial stromal cells.
围产期应激导致内源性皮质醇水平升高是产后牛子宫感染的危险因素之一。硒是一种微量元素，具有抗炎和抗氧化作用。本研究旨在揭示硒对高水平皮质醇存在下原代牛子宫内膜基质细胞炎症反应的调节作用。用脂多糖处理细胞以建立细胞炎症。用 qPCR 测量 toll 样受体 4（TLR4）、促炎因子和硒蛋白的 mRNA 表达。用 Western blot 和免疫荧光检测 NF-κB 和 MAPK 信号通路的激活。
亚硒酸钠（2 和 4 μM）预处理导致 TLR4 和编码促炎因子的基因下调，包括白细胞介素（IL）-1β、IL-6、IL-8、肿瘤坏死因子 α、环氧化酶 2 和诱导型一氧化氮合酶。硒抑制 NF-κB 的激活和丝裂原激活蛋白激酶激酶、细胞外信号调节激酶、p38MAPK 和 c-Jun N 末端激酶/应激激活蛋白激酶的磷酸化。在高皮质醇水平（30ng/mL）下，硒对这些基因和途径的抑制作用更为显著。同时，硒促进了谷胱甘肽过氧化物酶 1 和 4 的基因表达，并且在皮质醇和硒存在下更高。
硒的抗炎作用可能是通过 NF-κB 和 MAPK 介导的，并在原代牛子宫内膜基质细胞中被皮质醇增强。
