间歇性轻度寒冷适应通过调节TLR4/MyD88/NF-κB通路来改善急性寒冷压力 brojlers的肠道炎症和免疫功能障碍
Yanju Bi1, Haidong Wei2, Yiwen Chai2
1College of Veterinary Medicine, Northeast Agricultural University, 150030 Harbin, China.
Poultry science
|March 22, 2024
概括
温和的寒冷刺激通过减少炎症和氧化应激来保护肉肠免受急性寒冷压力. 这种预先条件调节了关键的免疫通路,改善了家禽的肠道健康和功能.
科学领域:
- 禽畜科学 禽畜科学 禽畜科学
- 动物生理学 动物生理学
- 免疫学 免疫学 免疫学
背景情况:
- 急性感冒压力 (ACS) 对肉肠道健康产生负面影响,导致炎症和氧化损伤.
- 了解防寒压力保护机制对于优化家禽福利和生产率至关重要.
研究的目的:
- 评估先前轻度寒冷刺激对肉肠道完整性和在急性寒冷压力下免疫功能的保护作用.
- 阐明涉及冷应激反应和减轻 brojlers 的分子途径.
主要方法:
- 肉接受了控制,急性寒冷应激 (ACS) 或轻度寒冷刺激 (低于正常的3°C或9°C),然后进行ACS.
- 分析了肠道组织的组织病理学,基因和蛋白质表达 (TLR4 / MyD88 / NF-κB通路,细胞因子,HSP) 和氧化应激标志物.
- 测量了sIgA度和抗氧化酶 (CAT,SOD,GSH-px) 的活性.
主要成果:
- ACS诱导肠道炎症,微虫损伤和密室深度增加,伴随着免疫基因表达变化和氧化应激.
- 温和的冷刺激 (3°C低于正常) 显著缓解了这些病理变化,并调节了基因表达,使其变得不那么炎症.
- 寒冷压力增加了氧化压力标志物 (MDA,H2O2) 和降低了抗氧化酶活动和sIgA,效应部分减轻了之前的寒冷刺激.
结论:
- 急性寒冷压力通过TLR4/MyD88/NF-κB通路在肉中引发氧化压力,炎症和肠道免疫功能障碍.
- 之前的轻度冷刺激 (降低3°C) 提供了保护作用,通过调节炎症和氧化途径来缓解肠道损伤和功能障碍.
- 这项研究突出了一个潜在的策略,通过受控的环境预先调节来增强肉对寒冷压力的抵抗力.
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