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Decreased enteritis resistance ability by dietary low or excess levels of lipids through impairing the intestinal physical and immune barriers function of young grass carp (Ctenopharyngodon idella)

机译:通过损害幼儿鲤鱼的肠道物理和免疫屏障功能(Ctenopharyncodon Idella),通过膳食低或过量脂质水平降低肠炎抗炎能力

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The current study explores the hypothesis that low or excess levels of lipids decrease the enteritis resistance ability through impairing the intestinal physical and immune barrier function of young grass carp (Ctenopharyngodon idella). A total of 540 young grass carp with an average initial weight of 261.41 +/- 0.53 g were fed diets containing six graded levels of lipids at 5.9, 21.4, 36.0, 50.2, 66.6 and 80.1 g/kg for 8 weeks. After that, a challenge trial was conducted by injection of Aeromonas hydrophila over 2 weeks. The results show that compared with optimal lipids level, low or excess levels of lipids impair fish immune barrier function through declining humoral compounds and down-regulating the mRNA levels of interleukin 4/13A (IL-4(13)A) [not in the proximal intestine (P0], IL-4(13)B, IL-6, IL-10, transforming growth factor beta 1 (TGF-beta 1), inhibitor of KB alpha (I kappa B alpha), TOR and ribosomal p70S6 kinase (S6K1) (P 0.05), and up-regulating tumor necrosis factor alpha (TNF-alpha), interferon gamma 2 (IFN-gamma 2), IL-1 beta, IL-8, IL-12 p40 (not p35), nuclear factor kappa B p65 (NF-kappa B p65), I kappa B kinase alpha (IKK alpha), IKK beta, IKK gamma, and elF4E-binding protein (4EBP) in the intestine of young grass carp (P 0.05). In addition, low or excess levels of lipids also decrease young grass carp physical barrier function through down-regulating the mRNA levels of zonula occludens (ZO-1), ZO-2b [only in the distal intestine (DI)], Claudin b, c, 3, 12, 15a, 15b (only in the DI), 7b (not 7a) and Occludin by MAPKK 6/p38 MAPK (not JNK)/MLCK signaling molecules, down-regulating B-cell lymphoma-2 (Bcl-2) and inhibitor of apoptosis protein (IAP) and up-regulating the mRNA levels of apoptotic protease activating factor-1 (Apaf-1), Caspase-3, -8 and -9 and Fas ligand (FasL) (not in the DI), and decreasing antioxidant ability via Kelch-like ECH-associating protein 1 (Keap1)/NF-E2-related factor 2 (Nrf2) signaling molecules in the intestine. Based on the quadratic regression analysis for the enteritis resistance ability, LA activities and GSH content in the MI were established to be 54.5, 49.91 and 47.83 g lipid/kg diets, respectively. (C) 2017 Elsevier Ltd. All rights reserved.
机译:目前的研究探讨了以下假设,脂质水平降低通过损害幼儿鲤鱼(Ctenopharyncodon Idella)的肠道物理和免疫屏障功能来降低肠炎抗炎能力。总共540只具有261.41 +/- 0.53g的初始重量的幼小草鲤鱼喂食含有六分级脂质的脂质的饮食,5.9,21.4,36.0,50.2,66.6和80.1g / kg持续8周。之后,通过在2周内注射Aeromonas患者的挑战试验。结果表明,与最佳脂质水平相比,脂质水平低或过量脂质损害鱼类免疫屏障函数,通过减少体液化合物和下调白细胞介素4 / 13a的mRNA水平(IL-4(13))[不在近端肠(P0],IL-4(13)B,IL-6,IL-10,转化生长因子β1(TGF-BETA 1),KBα(IκBα),TOR和核糖体P70S6激酶的抑制剂(S6K1)(P< 0.05),上调肿瘤坏死因子α(TNF-α),干扰素γ2(IFN-Gamma 2),IL-1β,IL-8,IL-12 P40(不是P35 ),核因子Kappa B p65(NF-Kappa B p65),I Kappa B激酶α(IKKα),IKKβ,IKKγ和ELF4E结合蛋白(4EBP)在幼小草鲤鱼的肠中(P L; 0.05)。此外,低或过量的脂质水平也通过降低ZONULA occludens(ZO-1),ZO-2B [仅在远端肠(DI)], Claudin B,C,3,12,15a,15b(只有i n Di),7b(不是7a)和MAPKK 6 / P38 MAPK(不是JNK)/ MLCK信号分子,下调B细胞淋巴瘤-2(BCL-2)和凋亡蛋白(IAP)的抑制剂和抑制剂Up-Crouse调节凋亡蛋白酶激活因子-1(APAF-1),Caspase-3,-8和-9和Fas配体(FasL)(不在DI中)的mRNA水平,并通过kelch样ech降低抗氧化能力 - 分配蛋白1(Keap1)/ NF-E2相关因子2(NRF2)信号传导分子在肠中。基于对肠炎抵抗能力的二次回归分析,MI中的LA活动和GSH含量分别建立为54.5,49.91和47.83g脂质/ kg饮食。 (c)2017 Elsevier Ltd.保留所有权利。

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