The immune system is one aspect of health that is affected by dietary selenium (Se) levels and selenoprotein expression. Spleen is an important immune organ of the body, which is directly involved in cellular immunity. However, there are limited reports on Se levels and spleen health. Therefore, this study established a Se-deficient pig model to investigate the mechanism of Se deficiency-induced splenic pathogenesis. Twenty-four pure line castrated male Yorkshire pigs (45 days old, 12.50 ± 1.32 kg, 12 full-sibling pairs) were divided into two equal groups and fed Se-deficient diet (0.007 mg Se/kg) or Se-adequate diet (0.3 mg Se/kg) for 16 weeks. At the end of the trial, blood and spleen were collected to assay for erythroid parameters, the osmotic fragility of erythrocytes, the spleen index, histology, terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) staining, Se concentrations, the selenogenome, redox status, and signaling related inflammation and apoptosis. Dietary Se deficiency decreased the erythroid parameters and increased the number of osmotically fragile erythrocytes (P < 0.05). The spleen index did not change, but hematoxylin and eosin and TUNEL staining indicated that the white pulp decreased, the red pulp increased, and splenocyte apoptosis occurred in the Se deficient group. Se deficiency decreased the Se concentration and selenoprotein expression in the spleen (P < 0.05), blocked the glutathione and thioredoxin antioxidant systems, and led to redox imbalance. Se deficiency activated the NF-κB and HIF-1α transcription factors, thus increasing pro-inflammatory cytokines (IL-1β, IL-6, IL-8, IL-17, and TNF-α), decreasing anti-inflammatory cytokines (IL-10, IL-13, and TGF-β) and increasing expression of the downstream genes COX-2 and iNOS (P < 0.05), which in turn induced inflammation. In addition, Se-deficiency induced apoptosis through the mitochondrial pathway, upregulated apoptotic genes (Caspase3, Caspase8, and Bak), and downregulated antiapoptotic genes (Bcl-2) (P < 0.05) at the mRNA level, thus verifying the results of TUNEL staining. These results indicated that Se deficiency induces spleen injury through the regulation of selenoproteins, oxidative stress, inflammation and apoptosis.

中文翻译：

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硒缺乏会通过降低硒蛋白表达，引起氧化应激以及激活炎症和凋亡来诱导猪的脾脏病理变化

免疫系统是健康的一个方面，受饮食中硒（Se）水平和硒蛋白表达的影响。脾脏是人体重要的免疫器官，直接参与细胞免疫。但是，关于硒水平和脾脏健康的报道很少。因此，本研究建立了硒缺乏猪模型，以研究硒缺乏引起的脾脏发病机理。将二十四只纯系去势的雄性约克郡pig割公猪（45天大，12.50±1.32千克，全兄弟姐妹对12对）分为两组，并饲喂低硒饮食（0.007毫克硒/千克）或低硒饮食（ 0.3 mg Se / kg），持续16周。在试验结束时，收集血液和脾脏以测定类红细胞参数，红细胞的渗透脆性，脾脏指数，组织学，末端脱氧核苷酸转移酶缺口末端标记（TUNEL）染色，硒浓度，硒基因组，氧化还原状态以及信号传导相关的炎症和细胞凋亡。饮食中硒缺乏会降低红系参数并增加渗透性脆性红细胞的数量（P <0.05）。脾虚组脾脏指数未改变，但苏木精和曙红及TUNEL染色显示白浆减少，红浆增加，脾细胞凋亡。硒缺乏会降低脾脏中硒的含量和硒蛋白的表达（P <0.05），阻断谷胱甘肽和硫氧还蛋白的抗氧化系统，并导致氧化还原失衡。硒缺乏激活了NF-κB和HIF-1α转录因子，从而增加了促炎性细胞因子（IL-1β，IL-6，IL-8，IL-17和TNF-α），降低抗炎细胞因子（IL-10，IL-13和TGF-β）并增加下游基因COX-2和iNOS的表达（P <0.05），从而引起炎症。此外，硒缺乏症通过线粒体途径诱导细胞凋亡，在mRNA水平上调凋亡基因（Caspase3，Caspase8和Bak）和下调抗凋亡基因（Bcl-2）（P <0.05），从而验证了TUNEL的结果。染色。这些结果表明，硒缺乏通过硒蛋白的调节，氧化应激，炎症和细胞凋亡引起脾损伤。在mRNA水平上调凋亡基因（Caspase3，Caspase8和Bak）和下调抗凋亡基因（Bcl-2）（P <0.05），从而验证了TUNEL染色的结果。这些结果表明，硒缺乏通过硒蛋白的调节，氧化应激，炎症和细胞凋亡引起脾损伤。在mRNA水平上调凋亡基因（Caspase3，Caspase8和Bak）和下调抗凋亡基因（Bcl-2）（P <0.05），从而验证了TUNEL染色的结果。这些结果表明，硒缺乏通过硒蛋白的调节，氧化应激，炎症和细胞凋亡引起脾损伤。