The role of selenoprotein W in inflammatory injury in chicken immune tissues and cultured splenic lymphocyte

The role of selenoprotein W in inflammatory injury in chicken immune tissues and cultured splenic lymphocyte
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DOI:
10.1007/s10534-014-9804-x
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发表时间:
2015-02
期刊:
影响因子:
3.5
通讯作者:
Dong Yu;Ziwei Zhang;Hai-dong Yao;Shu Li;Shiwen Xu
Dong Yu;Ziwei Zhang;Hai-dong Yao;Shu Li;Shiwen Xu
中科院分区:
生物学3区
文献类型:
--
作者:
Dong Yu;Ziwei Zhang;Hai-dong Yao;Shu Li;Shiwen Xu

文献摘要

相似文献

硒蛋白W(SelW)主要是根据其在细胞防御系统中的抗氧化作用来理解的。炎症是动物组织损伤的重要指标,并且炎症细胞可以触发复杂且精心策划的炎症级联反应,导致过度的氧化应激。为探讨硒蛋白(SelW)在鸡免疫组织和脾淋巴细胞炎症损伤中的作用,本实验观察了硒(Se)对鸡免疫组织和脾淋巴细胞中SelW和炎症因子mRNA表达的影响,(iNOS、考克斯-2、NF-κB、PTGEs和TNF-α)在鸡免疫器官中的表达(脾、胸腺和法氏囊)和培养的脾淋巴细胞用亚硒酸钠和H2 O2处理,或用小干扰RNA(siRNA)敲低SelW。结果表明,低硒饲料显著降低了SelW mRNA的表达(P< 0.05),并显著上调了考克斯-2、iNOS、NF-κB、PTGEs和TNF-α mRNA的表达(P< 0.05)。组织病理学分析表明,低硒组免疫组织有明显损伤。体外培养的脾淋巴细胞中,H2 O2可诱导炎症相关基因iNOS、考克斯-2、NF-κB、PTGEs和TNF-α的mRNA水平显著上调(P< 0.05)。用Se预处理后再用H_2O_2处理,可显著降低淋巴细胞炎症相关基因的表达(P< 0.05)。SelW基因沉默后,脾淋巴细胞炎症相关基因iNOS、考克斯-2、NF-κB、PTGEs和TNF-α表达显著上调(P< 0.05)。结果提示,硒可影响鸡肝脏炎症因子iNOS、考克斯-2、NF-κB、PTGEs、TNF-α和SelW的表达水平。SelW通过调控炎症相关基因的表达,在保护鸟类免疫器官免受炎症损伤中发挥重要作用。
Selenoprotein W (SelW) is mainly understood in terms of its antioxidant effects in the cellular defense system. Inflammation is an important indicator of animal tissue injury, and the inflammatory cells may trigger a sophisticated and well-orchestrated inflammatory cascade, resulting in exaggerated oxidative stress. To investigate the role of SelW in inflammatory injury in chicken immune tissues and cultured splenic lymphocyte, in this report, the effects of selenium (Se) on mRNA expressions of SelW and inflammatory factors (iNOS, COX-2, NF-κB, PTGEs, and TNF-α) in the chicken immune organs (spleen, thymus and bursa of Fabricius) and cultured splenic lymphocyte treated with sodium selenite and H2O2, or knocked down SelW with small interfering RNAs (siRNAs) were examined. The results showed that Se-deficient diets effectively decreased the mRNA expression of SelW (P< 0.05), and induced a significantly up-regulation of COX-2, iNOS, NF-κB, PTGEs and TNF-α mRNA levels (P< 0.05). The histopathological analysis showed that immune tissues were obviously injured in the low-Se groups. In vitro, H2O2induced a significantly up-regulation of the mRNA levels of inflammation-related genes (iNOS, COX-2, NF-κB, PTGEs, and TNF-α) in cultured splenic lymphocyte (P< 0.05). When lymphocytes were pretreated with Se before treated with H2O2, the inflammation-related genes were significantly decreased (P< 0.05). Silencing of SelW significantly up-regulated the inflammation-related genes (iNOS, COX-2, NF-κB, PTGEs, and TNF-α) in cultured splenic lymphocyte (P< 0.05). The results suggested that the expression levels of inflammatory factors (iNOS, COX-2, NF-κB, PTGEs, and TNF-α) and SelW can be influenced by Se in birds. SelW commonly played an important role in the protection of immune organs of birds from inflammatory injury by the regulations of inflammation-related genes.