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揭示过多的料来源导致中的铜诱导性乳头炎:洞察紧接点损伤和ROS/NLRP3/pyroptosis轴的洞察

Boran Zhou¹, Yufei Cao¹, Yingxue Zhang¹

¹College of Wildlife and Protected Area, Northeast Forestry University, Harbin, 150040, Heilongjiang, PR China.

Comparative biochemistry and physiology. Toxicology & pharmacology : CBP

|September 15, 2025

概括

肉料中过量的铜会通过激活ROS-NLRP3轴,导致炎症和热,导致肠道毒性. 这会损害肠道屏障,凸显了畜牧业中高铜水平的风险.

科学领域:

动物科学动物科学
毒理学毒理学毒理学
免疫学免疫学免疫学

背景情况:

硫酸铜 (CuSO4) 在牲畜料中广泛用于促进生长和抗菌作用.
过度的铜积累会导致肠道毒性,但肉中铜诱导的乳头炎的机制尚不清楚.

研究的目的:

阐明铜诱导的肠道炎症和肉中毒性的机制.
研究反应性氧物种 (ROS) 和NLRP3炎症酶在铜毒性的作用.

主要方法:

在5周的时间里,肉被养为含有0,100或300毫克/公斤CuSO4的食.
评估了抗氧化防御,NLRP3炎症酶激活,炎症亡标记物,促炎媒介物,紧结蛋白和Wnt/β-catenin通路.

主要成果:

高铜量 (300 mg/kg) 抑制了抗氧化防御 (HO-1,NQO1,SOD,GSH-Px),但增加了催化酶 (CAT).
激活了NLRP3炎症酶和热致死标记物 (Caspase-1,IL-1β),表明ROS-NLRP3轴的参与.
调节失调的促炎媒介 (IL-7,IL-17,iNOS,TNF-α),降低了紧结蛋白 (ZO-1,Claudin-3,Occludin),并抑制了Wnt/β-catenin通路.

结论:

牛肉中铜诱导的肠炎和烧死是由ROS-NLRP3轴激活的介导.
铜的毒性损害了肠道粘膜屏障的完整性.
过度接触铜对肉健康构成重大风险.

关键词:

铜铜铜铜铜铜眼皮炎眼皮炎在ROS/NLRP3/pyroptosis轴上紧密的结口紧密的结口.

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