通过高皮质醇背景的Nrf2通路抑制了牛子宫内膜层细胞的LPS诱导的氧化应激
Luying Cui1,2,3, Fangling Zheng1,2,3, Min Zhang1,2,3
1College of Veterinary Medicine, Yangzhou University, Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Disease and Zoonoses, Yangzhou, Jiangsu, PR China.
Journal of animal science
|September 2, 2024
概括
(Se) 保护牛子宫内膜细胞免受感染和压力引起的氧化应激. 补充剂,特别是在高皮质醇条件下,通过激活Nrf2通路来增强抗氧化能力.
科学领域:
- 生殖生物学 生殖生物学
- 细胞生理学 细胞生理学
- 营养生物化学 营养生物化学
背景情况:
- 周产压力和感染对奶牛的生殖健康产生负面影响.
- 由于压力导致皮质醇水平升高,可能会加剧子宫疾病.
- 已知 (Se) 可以增强牛的抗氧化能力.
研究的目的:
- 为了研究 (Se) 对牛初级子宫内膜层细胞 (BESC) 氧化应激的影响.
- 在高皮质醇条件下以及在脂多糖 (LPS) 存在的情况下,探索Se在BESC中的作用.
- 阐明Nrf2通路对BESC中Se介导的抗氧化作用的参与.
主要方法:
- 培养的初级牛子宫内膜层细胞 (BESC).
- 使用脂聚糖 (LPS) 和高皮质醇水平诱导的氧化应激.
- 测量了反应性氧物种 (ROS),马隆迪化物 (MDA) 和超氧化物溶解酶 (SOD) 的水平.
- 通过Western blot,qPCR和免疫光分析了Nrf2通路.
主要成果:
- 在BESC中,LPS诱导了显著的氧化应激,增加了ROS和MDA,同时减少了SOD.
- 高皮质醇水平增加了ROS和MDA,但在LPS刺激的细胞中显示出抗氧化作用.
- 预处理减少了氧化应激标志物 (ROS,MDA) 和增强了抗氧化能力 (SOD).
- 在高皮质醇条件下,Se提高了Nrf2通路的调节,其效果在高皮质醇条件下更为明显.
- 皮质醇单独诱导氧化损伤,但提供了对LPS诱导的压力的保护.
结论:
- 有效地减轻牛子宫内膜细胞中脂聚糖诱导的氧化应激,可能是通过Nrf2通路激活.
- 高皮质醇水平具有双重效应,诱导氧化损伤,但对LPS诱导的压力提供一些保护.
- 补充剂显示出对牛子宫内膜氧化损伤的显著保护作用,特别是在高皮质醇的压力动物中.
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