Deficiency of selenium (Se), an important trace element, causes diarrhea and even death in broilers, thereby affecting the economic development of poultry production. Adding Se is one way to relieve this situation; however, it has not fundamentally resolved intestinal inflammation. Therefore, we sought a new strategy to alleviate intestinal inflammation by studying the specific mechanisms of Se deficiency. By replicating the Se-deficient broiler model and establishing a chicken small intestinal epithelial cell (CSIEC) model, we determined that Se deficiency caused intestinal oxidative stress and necroptotic intestinal inflammation in broilers by decreasing glutathione peroxidase (GPX) 3 expression. Simultaneously, the expression of long non-coding RNA (lncRNA)WSF27 decreased and that of miR-1696 increased in Se-deficient intestines. Recently discovered competing endogenous RNAs (ceRNAs) form novel regulatory networks, which were found that selenoproteins involved in ceRNA regulation. However, the mechanism of action of the non-coding RNA/GPX3 axis in Se-deficient broiler intestinal inflammation remains unclear. This study aimed to explore the mechanism through which Se deficiency regulates intestinal inflammation in broilers through the lncRNAWSF27/miR-1696/GPX3 axis. Our previous studies showed that lncRNAWSF27, miR-1696, and GPX3 have ceRNA-regulatory relationships. To further determine the role of the lncRNAWSF27/miR-1696/GPX3 axis in Se-deficient broiler intestinal inflammation, CSIEC models with GPX3 knockdown/overexpression, lncRNAWSF27 knockdown, or miR-1696 knockdown/overexpression were established to simulate intestinal injury. GPX3 knockdown, as well as lncRNAWSF27 and miR-1696 overexpression, aggravated cell damage. On the contrary, it can alleviate this situation. Our results reveal that mechanism of lncRNAWSF27/miR-1696/GPX3 regulated Se-deficient broiler intestinal inflammation. This conclusion enriches our understanding of the mechanism of intestinal injury caused by Se deficiency, and contributes to the diagnosis of Se-deficient intestinal inflammation and relevant drug development.

中文翻译：

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缺硒通过 lncRNAWSF27/miRNA1696/GPX3 轴调节肉鸡坏死性凋亡介导的肠道炎症。


重要的微量元素硒（Se）缺乏会导致肉鸡腹泻甚至死亡，从而影响家禽生产的经济发展。添加硒是缓解这种情况的一种方法；但并没有从根本上解决肠道炎症。因此，我们通过研究硒缺乏的具体机制，寻求缓解肠道炎症的新策略。通过复制缺硒肉鸡模型并建立鸡小肠上皮细胞（CSIEC）模型，我们确定缺硒通过降低谷胱甘肽过氧化物酶（GPX）3表达而导致肉鸡肠道氧化应激和坏死性肠道炎症。同时，缺硒肠道中长非编码RNA (lncRNA)WSF27 的表达下降，miR-1696 的表达增加。最近发现竞争性内源RNA（ceRNA）形成新的调控网络，其中发现硒蛋白参与ceRNA调控。然而，非编码RNA/GPX3轴在缺硒肉鸡肠道炎症中的作用机制仍不清楚。本研究旨在探讨硒缺乏通过lncRNAWSF27/miR-1696/GPX3轴调节肉鸡肠道炎症的机制。我们之前的研究表明lncRNAWSF27、miR-1696和GPX3具有ceRNA调控关系。为了进一步确定lncRNAWSF27/miR-1696/GPX3轴在缺硒肉鸡肠道炎症中的作用，建立了GPX3敲低/过表达、lncRNAWSF27敲低或miR-1696敲低/过表达的CSIEC模型来模拟肠道损伤。 GPX3 敲低以及 lncRNAWSF27 和 miR-1696 过度表达，加剧了细胞损伤。 相反，可以缓解这种情况。我们的结果揭示了lncRNAWSF27/miR-1696/GPX3调节缺硒肉鸡肠道炎症的机制。该结论丰富了我们对缺硒引起肠道损伤机制的认识，有助于缺硒肠道炎症的诊断及相关药物的研发。