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首页> 外文期刊>RSC Advances >SelW protects against H2O2-induced liver injury in chickens via inhibiting inflammation and apoptosis
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SelW protects against H2O2-induced liver injury in chickens via inhibiting inflammation and apoptosis

机译：SelW通过抑制发炎和凋亡来预防H 2 O 2 引起的鸡肝损伤

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Selenium (Se) is recognized as a necessary trace mineral in animal diets. Se deficiency induces a number of diseases and injuries in chickens including liver damage, which is related to oxidative stress. Selenoprotein?W (SelW) plays a crucial role in antioxidant defense mechanisms in mammals; however, little is known about the role of SelW and cytokines in H2O2-mediated chicken liver damage since chicken SelW has no cysteine (Cys) at residue 37 (Cys37) that is required for its presumed antioxidant function in mammals. The aim of this study was to evaluate whether chicken SelW possessed the same function as mammal SelW and to investigate the protective role of SelW against H2O2 by influencing the expression of inflammation and apoptosis via building a model of overexpressed or/and knocked down SelW in cultured chicken hepatic cells. The results showed that after the cells were exposed to H2O2, the levels of P53, caspase-3, Bax, Bak, COX-2, PTGEs, TNF-α, iNOS and NF-κB were lower in the SelW overexpressed cells but higher in the SelW knockdown cells compared to the H2O2-only treatment group. However, the result for Bcl-2 was opposite to that of the other apoptosis-promoting genes. Moreover, chickens were fed with a Se-deficient diet containing 0.032 mg kg?1 Se for 15, 25, 35, 45, and 55 days, and their liver tissues were collected and examined for apoptosis and inflammation. The results showed that the levels of P53, Bax, Bak, COX-2, PTGEs, TNF-α, iNOS and NF-κB in the Se-deficient chicken livers were dramatically higher than the levels in the normal control group. In conclusion, our findings suggested that chicken SelW possess an antioxidant function similar to the mammalian homologs despite the lack of Cys37 in the peptide, and SelW regulated related-inflammation and apoptosis during H2O2-dependent chicken liver damage.
机译：硒（Se）被认为是动物饮食中必需的微量矿物质。硒缺乏会引起鸡多种疾病和伤害，包括肝损伤，这与氧化应激有关。硒蛋白？W（SelW）在哺乳动物的抗氧化防御机制中起着至关重要的作用。然而，关于SelW和细胞因子在H 2 O 2 介导的鸡肝损伤中的作用了解甚少。因为鸡肉SelW在其残留37（Cys37）上没有半胱氨酸（Cys），这在哺乳动物中可能是其抗氧化功能所必需的。这项研究的目的是评估鸡肉SelW是否具有与哺乳动物SelW相同的功能，并研究SelW对H 2 O 的保护作用。 2 通过建立培养的鸡肝细胞中SelW的过表达或/和敲低模型来影响炎症和凋亡的表达。结果显示，细胞暴露于H 2 O 2 后，P53，caspase- 3，与H 2 相比，SelW过表达细胞中Bax，Bak，COX-2，PTGEs，TNF-α，iNOS和NF-κB较低，而SelW击倒细胞中较高。仅 O 2 治疗组。但是，Bcl-2的结果与其他凋亡促进基因的结果相反。此外，给鸡饲喂含硒量为0.032 mg kg ？1 的硒缺乏饲料，持续15、25、35、45和55天，它们的肝脏组织收集并检查细胞凋亡和炎症。结果表明，缺硒鸡肝中P53，Bax，Bak，COX-2，PTGEs，TNF-α，iNOS和NF-κB的水平显着高于正常对照组。总之，我们的发现表明，尽管肽中缺少Cys37，但鸡SelW具有与哺乳动物同源物相似的抗氧化功能，并且SelW在H 2 期间调节相关炎症和细胞凋亡。 small> O 2 依赖性鸡肝损伤。

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