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缺乏症通过lncRNAWSF27/miRNA1696/GPX3轴调节肉中死菌中介的肠炎症

Yiming Zhang¹, Chunyu Wei¹, Jiayi Ding¹

¹College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, P. R. China.

Journal of animal science

|September 27, 2024

概括

肉中的缺乏会通过氧化应激和亡引起肠道炎症. 这项研究确定了lncRNAWSF27/miR-1696/GPX3轴作为一个关键的监管机制,为家禽生产提供了新的诊断和治疗目标.

科学领域:

分子生物学分子生物学
动物营养动物营养
禽畜科学禽畜科学禽畜科学

背景情况:

肉中的 (Se) 缺乏导致严重的肠道问题,包括腹和炎症,影响家禽生产经济.
目前的Se补充策略不能完全解决肠道炎症,需要对潜在的分子机制有更深入的了解.
氧化应激和丧尸症与Se缺乏引起的肠损伤有关.

研究的目的:

阐明Se缺乏导致 brojlers肠道炎症的特定分子机制.
研究长非编码RNA (lncRNA) WSF27/miR-1696/glutathione peroxidase (GPX3) 轴在Se缺乏性肠道炎症中的作用.
探索针对这一监管轴的潜在诊断和治疗策略.

主要方法:

建立Se缺乏的肉和小肠上皮细胞 (CSIEC) 模型.
对基因和微RNA表达的分析,包括lncRNAWSF27,miR-1696和GPX3.
在CSIEC模型中操纵GPX3,lncRNAWSF27和miR-1696的表达 (敲击/过度表达),以评估它们对细胞损伤的影响.

主要成果:

缺少Se减少了GPX3的表达,导致牛肉的氧化应激和死菌性肠炎症.
缺少Se改变了lncRNAWSF27 (减少) 和miR-1696 (增加) 的表达,这表明它们参与了调节网络.
GPX3敲除和lncRNAWSF27/miR-1696过度表达加剧了细胞损伤,而它们相反的操纵减轻了细胞损伤,证实了轴的作用.

结论:

lncRNAWSF27/miR-1696/GPX3轴是Se缺乏肉肠炎症的关键调节者.
这项研究揭示了一种新的ceRNA调节网络,有助于Se缺乏引起的肠损伤.
这些发现为制定针对家禽的Se缺乏性肠炎的有针对性的干预措施提供了基础.

关键词:

我们的LncRNAWSF27/miR-1696/GPX3 brojler 肉肉是一个肠道炎症是一种肠道炎症.尸体的死亡和死亡的死亡.是一种.

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