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音乐干预通过TLR4/NF-κB调节减轻脂多糖诱导的肉鸡肠道屏障破坏和免疫应激。

Music intervention mitigates LPS-induced gut barrier disruption and immune stress in broilers via TLR4/NF-κB regulation.

作者信息

Jin Shengzi, Wang Haowen, Gong Haiyue, Guo Lu, Zhang Haoran, Zhang Jiaqi, Chang Qingqing, Li Jianhong, Zhang Runxiang, Bao Jun

机构信息

College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, PR China.

Department of Basic Medical Sciences, Heilongjiang Nursing College, Harbin, Heilongjiang 150086, China.

出版信息

Poult Sci. 2025 Apr 22;104(7):105189. doi: 10.1016/j.psj.2025.105189.

Abstract

Immune stress induced by harsh environment in intensive farming can impair broiler intestinal health. Although music as an environmental intervention can alleviate short-term stress injury, its long-term regulatory mechanism on intestinal inflammation has not been clarified. In this study, we investigated the effects of a music-enriched environment on growth performance, intestinal barrier function, and inflammatory responses in lipopolysaccharide (LPS)-induced immunostressed broilers. AA broilers were randomly divided into four groups: control group (CON), music-enriched environment group (MUC), LPS-induced immune stress group (LPS) and music-enriched environment + LPS group (MUC+LPS). On the 14th, 16th and 18th days, the LPS and MUC+LPS groups were injected intraperitoneally with 500 μg of LPS to construct an immune stress model, and the CON and MUC groups were injected with an equal amount of saline. On day 28, the birds were sacrificed to detect the indicators associated with intestinal barrier and inflammation. The LPS group showed a significant decrease in performance from 14 to 28 days, with elevated serum levels of CORT, ACTH, DAO, and d-LA, and a decrease in the activity of intestinal mucosal SOD/GSH-Px, and impaired gut morphology. impaired; music remission significantly alleviated the decline in production performance, reduced the levels of stress hormones and markers of intestinal barrier damage, while elevating jejuno-ileal GSH-Px activity and improving intestinal morphology. Significant inflammatory gene expression characteristics were observed in jejunum and ileum tissues after LPS injection: upregulation of TLR4, NF-κB, TNF-α, IL-1β, and IL-6, and significant suppression of jejunal IL-10 expression. Notably, IL-10 and IFN-γ expression in the ileum did not show statistical differences. Inflammation-related gene expression showed an overall down-regulation trend after the music intervention, but was still significantly different from the control group. Music intervention on the regulation of jejunal MYD88 and ileal TNF-α - the LPS group did not show statistically significant differences in the expression of these two key inflammatory nodes with the LPS+MUS group. Mechanistic studies have shown that LPS triggers an oxidative stress cascade through activation of the TLR4/NF-κB signaling axis, leading to disruption of intestinal barrier integrity. In contrast, music exposure exerts a protective effect through a dual mechanism: on the one hand, it helps to enhance the expression of the tight junction protein ZO-1/Occludin to repair the physical barrier; on the other hand, it inhibits the activation of the TLR4/NF-κB pathway, which can effectively alleviate LPS-induced immunopathological damage.

摘要

集约化养殖中恶劣环境诱导的免疫应激会损害肉鸡肠道健康。尽管音乐作为一种环境干预手段可以缓解短期应激损伤,但其对肠道炎症的长期调节机制尚未阐明。在本研究中,我们调查了富含音乐的环境对脂多糖(LPS)诱导的免疫应激肉鸡生长性能、肠道屏障功能和炎症反应的影响。AA肉鸡被随机分为四组:对照组(CON)、富含音乐的环境组(MUC)、LPS诱导的免疫应激组(LPS)和富含音乐的环境 + LPS组(MUC+LPS)。在第14、16和18天,LPS组和MUC+LPS组腹腔注射500μg LPS以构建免疫应激模型,CON组和MUC组注射等量生理盐水。在第28天,处死鸡只以检测与肠道屏障和炎症相关的指标。LPS组在第14至28天性能显著下降,血清CORT、ACTH、DAO和d-LA水平升高,肠黏膜SOD/GSH-Px活性降低,肠道形态受损;音乐缓解显著减轻了生产性能的下降,降低了应激激素水平和肠道屏障损伤标志物,同时提高了空肠-回肠GSH-Px活性并改善了肠道形态。LPS注射后,空肠和回肠组织中观察到显著的炎症基因表达特征:TLR4、NF-κB、TNF-α、IL-1β和IL-6上调,空肠IL-10表达显著受抑制。值得注意的是,回肠中IL-10和IFN-γ表达未显示统计学差异。音乐干预后炎症相关基因表达总体呈下调趋势,但仍与对照组有显著差异。音乐干预对空肠MYD88和回肠TNF-α的调节——LPS组与LPS+MUS组在这两个关键炎症节点的表达上未显示统计学显著差异。机制研究表明,LPS通过激活TLR4/NF-κB信号轴触发氧化应激级联反应,导致肠道屏障完整性破坏。相比之下,音乐暴露通过双重机制发挥保护作用:一方面,它有助于增强紧密连接蛋白ZO-1/Occludin的表达以修复物理屏障;另一方面,它抑制TLR4/NF-κB途径的激活,从而有效减轻LPS诱导的免疫病理损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ae4/12059385/8b56292f87c3/gr1.jpg

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