Selenium (Se) is an important nutritional element in the diet. Apoptosis is one of the characteristic pathological changes in liver tissue resulting from Se deficiency. MicroRNA (miRNA) plays an important role in cell proliferation, differentiation, apoptosis and tumorigenesis. However, why apoptosis occurs during Se deficiency and how miRNA regulates hepatocyte apoptosis in broilers requires further study. We used a dual luciferase reporter assay system and quantitative real-time PCR (qPCR) to screen hepatocytes in Se-deficient broilers for the specificity of hepatocyte apoptosis miRNA and its target protein. We tested the apoptosis of Se-deficient broiler livers and microRNA-193b-transfected primary hepatocytes using qPCR, western blot (WB) and flow cytometry. Our studies revealed that Se deficiency led to microRNA-193b-3p (miR-193b-3p) overexpression and increased apoptosis-related gene expression, resulting in broiler hepatocyte apoptosis. Mastermind-like protein 1 (MAML1) was one of the miR-193b-3p targets, and its expression was down-regulated in miR-193b-3p-overexpressing hepatocytes. Further studies have shown that miR-193b-3p overexpression induced changes of apoptosis-related gene expression by inhibiting the release of MAML1. Interestingly, when we overexpressed miR-193b-3p, which was added to the Signal transducers and activators of transcription-1 (STAT1) inhibitor fludarabine (Flu), hepatocyte apoptosis was significantly reduced. When these results were combined, they indicated that miR-193b-3p is involved in broiler hepatocyte apoptosis in Se deficiency by regulating the target protein MAML1. This finding may provide new ideas for studying the mechanism of hepatocyte injury due to Se deficiency.

硒是饮食中重要的营养元素。凋亡是由硒缺乏引起的肝组织的特征性病理变化之一。MicroRNA（miRNA）在细胞增殖，分化，凋亡和肿瘤发生中起重要作用。但是，为什么在硒缺乏期间发生凋亡，以及miRNA如何调节肉鸡的肝细胞凋亡尚待进一步研究。我们使用双重荧光素酶报告基因检测系统和定量实时PCR（qPCR）筛选硒缺乏型肉鸡中肝细胞的肝细胞凋亡miRNA及其靶蛋白的特异性。我们使用qPCR，western blot（WB）和流式细胞仪检测了Se缺乏的肉鸡肝脏和microRNA-193b转染的原代肝细胞的凋亡。我们的研究表明，硒缺乏会导致microRNA-193b-3p（miR-193b-3p）过表达并增加凋亡相关基因的表达，从而导致肉鸡肝细胞凋亡。Mastermind-like蛋白1（MAML1）是miR-193b-3p的靶标之一，在过表达miR-193b-3p的肝细胞中其表达下调。进一步的研究表明，miR-193b-3p的过表达通过抑制MAML1的释放来诱导凋亡相关基因表达的变化。有趣的是，当我们过表达miR-193b-3p（将其添加到信号转导和转录激活因子1（STAT1）抑制剂氟达拉滨（Flu））中时，肝细胞凋亡显着减少。当这些结果结合在一起时，他们指出，miR-193b-3p通过调节靶蛋白MAML1参与了硒缺乏症中的肉鸡肝细胞凋亡。这一发现可能为研究硒缺乏引起的肝细胞损伤机制提供新思路。