College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China.
College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China; Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China.
Comp Biochem Physiol C Toxicol Pharmacol. 2023 Feb;264:109504. doi: 10.1016/j.cbpc.2022.109504. Epub 2022 Nov 12.
Selenoprotein K (SELENOK) is a major part of selenoprotein family. Selenoproteins have been proven playing vital roles in a variety of physiological processes. However, as a necessary supplement to the body of trace elements, how SELENOK regulates necroptosis in chicken liver has none clear claim. The purpose of this study was to cover the mechanism of SELENOK act in necroptosis of chicken liver. By feeding Se-deficiency diet for 1-day-old hyline chickens, we successfully built SELENOK-deficiency and discussed the regulation SELENOK have done. The test of liver function showed there has dysfunction appeared in the -Se groups. Results of TEM showed necroptosis occurred in the 35-Se group. After that western blot and qRT-PCR results prompted us SELENOK-deficiency caused large accumulation of ROS, enhanced endoplasmic reticulum stress, abnormally elevated HSPs family expression, and activated RIPK1-RIPK3 complex. In order to show the regulation of SELENOK in chicken liver, we artificially knocked off SELENOK gene in LMH cells. Through AO/EB staining we also found necroptosis in the siRNA-Se group. Furthermore, the results in LMH cells were coincided with those in chicken (Gallus gallus) liver. Our experiment clarified the molecular mechanism of SELENOK in the regulation and liver necroptosis, and provided reference for the healthy feeding mode of broilers.
硒蛋白 K（SELENOK）是硒蛋白家族的主要成员。硒蛋白已被证明在多种生理过程中发挥着重要作用。然而，作为人体微量元素的必需补充物，SELENOK 如何调节鸡肝细胞的坏死性凋亡尚不清楚。本研究旨在探讨 SELENOK 在鸡肝细胞坏死性凋亡中的作用机制。通过给 1 日龄海兰鸡喂食缺硒饮食，成功构建了 SELENOK 缺乏模型，并探讨了 SELENOK 的调节作用。肝功能测试显示，-Se 组出现了肝功能异常。TEM 结果显示 35-Se 组发生了坏死性凋亡。随后的 Western blot 和 qRT-PCR 结果表明，SELENOK 缺乏导致大量 ROS 积累、内质网应激增强、HSPs 家族表达异常升高，并激活了 RIPK1-RIPK3 复合物。为了展示 SELENOK 在鸡肝中的调节作用，我们在 LMH 细胞中人工敲除了 SELENOK 基因。通过 AO/EB 染色，我们还发现 siRNA-Se 组发生了坏死性凋亡。此外，LMH 细胞中的结果与鸡（Gallus gallus）肝中的结果一致。本实验阐明了 SELENOK 在调节和鸡肝坏死性凋亡中的分子机制，为肉鸡的健康饲养模式提供了参考。
