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通过损害草鱼幼鱼的肠道物理屏障和免疫屏障功能,饮食中低水平或过量的脂质会降低草鱼对肠炎的抵抗力。

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).

作者信息

Feng Lin, Ni Pei-Jun, Jiang Wei-Dan, Wu Pei, Liu Yang, Jiang Jun, Kuang Sheng-Yao, Tang Ling, Tang Wu-Neng, Zhang Yong-An, Tang Xu, Shi He-Qun, Zhou Xiao-Qiu

机构信息

Animal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, China; Fish Nutrition and Safety Production University Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu 611130, China; Key Laboratory for Animal Disease-Resistance Nutrition of China Ministry of Education, Sichuan Agricultural University, Chengdu 611130, China.

Animal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, China.

出版信息

Fish Shellfish Immunol. 2017 Aug;67:493-512. doi: 10.1016/j.fsi.2017.06.041. Epub 2017 Jun 16.

Abstract

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 (PI)], IL-4(13)B, IL-6, IL-10, transforming growth factor β1 (TGF-β1), inhibitor of κBα (IκBα), TOR and ribosomal p70S6 kinase (S6K1) (P < 0.05), and up-regulating tumor necrosis factor α (TNF-α), interferon γ2 (IFN-γ2), IL-1β, IL-8, IL-12 p40 (not p35), nuclear factor κB p65 (NF-κB p65), IκB kinase α (IKKα), IKKβ, IKKγ, and eIF4E-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.

摘要

本研究探讨了以下假说

低水平或过量的脂质会通过损害草鱼幼鱼(Ctenopharyngodon idella)的肠道物理屏障和免疫屏障功能,降低其抗肠炎能力。选取540尾初始平均体重为261.41±0.53 g的草鱼幼鱼,投喂含5.9、21.4、36.0、50.2、66.6和80.1 g/kg六个梯度脂质水平的饲料,持续8周。之后,通过注射嗜水气单胞菌进行为期2周的攻毒试验。结果表明,与最佳脂质水平相比,低水平或过量的脂质会通过降低体液化合物含量和下调白细胞介素4/13A(IL-4(13)A)[不在近端肠道(PI)中]、IL-4(13)B、IL-6、IL-10、转化生长因子β1(TGF-β1)、κBα抑制因子(IκBα)、TOR和核糖体p70S6激酶(S6K1)的mRNA水平,损害鱼类免疫屏障功能(P<0.05),并上调草鱼幼鱼肠道中肿瘤坏死因子α(TNF-α)、干扰素γ2(IFN-γ2)、IL-1β、IL-8、IL-12 p40(非p35)、核因子κB p65(NF-κB p65)、IκB激酶α(IKKα)、IKKβ、IKKγ和eIF4E结合蛋白(4EBP)的mRNA水平(P<0.05)。此外,低水平或过量的脂质还会通过下调紧密连接蛋白(ZO-1)、ZO-2b[仅在远端肠道(DI)中]、Claudin b、c、3、12、15a、15b(仅在DI中)、7b(非7a)和闭合蛋白的mRNA水平,通过MAPKK 6/p38 MAPK(非JNK)/MLCK信号分子降低草鱼幼鱼的物理屏障功能,下调B细胞淋巴瘤-2(Bcl-2)和凋亡抑制蛋白(IAP),上调凋亡蛋白酶激活因子-1(Apaf-1)、半胱天冬酶-3、-8和-9以及Fas配体(FasL)(不在DI中)的mRNA水平,并通过肠道中的Kelch样ECH相关蛋白1(Keap1)/NF-E2相关因子2(Nrf2)信号分子降低抗氧化能力。基于对肠炎抵抗能力的二次回归分析,确定中肠中LA活性和GSH含量的适宜脂质水平分别为54.5、49.91和47.83 g脂质/kg饲料。

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