急性寒冷压力通过CIRP-TLR4-IRE1信号通路诱导肠道损伤,在预启动肉中
Juanjuan Wu1, Guiyao Li1, Haoneng Guo1
1College of Animal Science and Technology, Jiangxi Agriculture University, Nanchang, 330045, Jiangxi, China.
Molecular biology reports
|May 30, 2023
概括
肉的急性寒冷压力会通过激活冷诱导性RNA结合蛋白 (CIRP) -Toll-like受体4 (TLR4) -IRE1通路来损害肠道,从而导致内质网膜压力.
科学领域:
- 动物科学动物科学
- 生理学 生理学 生理学
- 分子生物学分子生物学
背景情况:
- 寒冷压力对肉来说是一个重大的环境挑战.
- 冷诱导型RNA结合蛋白 (CIRP) 通过托尔类受体4 (TLR4) 参与炎症反应.
- 对于CIRP在 brojler冷压中的确切作用仍在调查中.
研究的目的:
- 为了研究CIRP-TLR4-IRE1信号通路在遭受急性寒冷压力的肉小中的参与.
- 评估寒冷压力对肠道完整性和内质网膜压力标记物的影响.
主要方法:
- 360只肉被暴露在急性寒冷 (12±1°C) 中,持续时间为0,4,8或12小时.
- 测量包括腹部皮肤温度,基因表达 (CIRP,TLR4,IRE1通路,炎症因素,紧结蛋白) 和小肠形态.
主要成果:
- 寒冷暴露降低了腹部皮肤温度,并诱导了内细胞网膜应激 (ERS) 标志物 (IRE1,GRP78).
- 炎症因子 (IL-1β,IL-6,IL-10,TNF-α) 和紧结蛋白 (ZO-1,Occludin) 的基因表达被上调.
- 长时间暴露于寒冷会增加CIRP和TLR4的表达,同时降低小的高度和小/密室 (V/C) 比率.
结论:
- 急性寒冷压力会在肉小中引发细胞内膜网膜压力.
- 在冷应力过程中,CIRP-TLR4-IRE1信号通路受到上调.
- 寒冷压力导致小小肠的结构损伤.
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