Selenium deficiency induces spleen pathological changes in pigs by decreasing selenoprotein expression, evoking oxidative stress, and activating inflammation and apoptosis.
Selenium deficiency induces spleen pathological changes in pigs by decreasing selenoprotein expression, evoking oxidative stress, and activating inflammation and apoptosis.
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硒缺乏通过降低硒蛋白表达、引起氧化应激、激活炎症和细胞凋亡等途径诱导猪脾脏病理改变。
DOI：
10.1186/s40104-021-00587-x
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发表时间：
2021-05-17
影响因子：
7
通讯作者：
Zhang J
中科院分区：
文献类型：
--
作者：
Li S;Sun W;Zhang K;Zhu J;Jia X;Guo X;Zhao Q;Tang C;Yin J;Zhang J
免疫系统是健康的一个方面，受饮食硒（Se）水平和硒蛋白表达的影响。脾脏是机体重要的免疫器官，直接参与细胞免疫。然而，关于硒水平和脾脏健康的报道有限。因此，本研究建立了低硒猪模型，探讨了低硒致脾脏病变的机制。选用24头45日龄纯系去势雄性约克郡猪（体重12.50 ± 1.32 kg，全同胞12对），随机分为两组，分别饲喂低硒（0.007 mg Se/kg）和高硒（0.3 mg Se/kg）日粮16周。试验结束时，采集血液和脾脏以测定红细胞参数、红细胞渗透脆性、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、氧化还原状态以及与炎症和凋亡相关的信号传导。低硒使红细胞参数降低，脆性红细胞数增加（P < 0.05）。脾指数无明显变化，但苏木精-伊红染色和TUNEL染色显示低硒组脾细胞白色髓减少，红髓增多，脾细胞凋亡。缺硒可降低脾脏硒含量和硒蛋白表达（P < 0.05），阻断谷胱甘肽和硫氧还蛋白抗氧化系统，导致氧化还原失衡。缺硒可激活NF-κB和HIF-1α转录因子，从而增加促炎细胞因子（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），并增加下游基因考克斯-2和iNOS的表达（P < 0.05），进而诱导炎症反应。此外，硒缺乏通过线粒体途径诱导细胞凋亡，在mRNA水平上调凋亡基因Caspase 3、Caspase 8和巴克，下调抗凋亡基因Bcl-2（P < 0.05），从而验证了TUNEL染色的结果。上述结果表明，硒缺乏通过调节硒蛋白、氧化应激、炎症反应和细胞凋亡等途径诱导脾脏损伤。在线版本包含补充材料，可通过10.1186/s40104-021-00587-x获得。
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. The online version contains supplementary material available at 10.1186/s40104-021-00587-x.
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影响因子：
4.8
作者：
Dharshini, Loganathan Chandramani Priya;Vishnupriya, Selvaraj;Rasmi, Rajan Radha
通讯作者：
Rasmi, Rajan Radha
影响因子：
3.9
作者：
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通讯作者：
Kaushal, Naveen
影响因子：
6.6
作者：
Kaushal, Naveen;Hegde, Shailaja;Prabhu, K. Sandeep
通讯作者：
Prabhu, K. Sandeep
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影响因子：
4.7
作者：
Chen, Hongxing;Li, Jian;Xie, Lingtian
通讯作者：
Xie, Lingtian
影响因子：
5.9
作者：
Avery JC;Hoffmann PR
通讯作者：
Hoffmann PR