Dietary myo-inositol modulates immunity through antioxidant activity and the Nrf2 and E2F4/cyclin signalling factors in the head kidney and spleen following infection of juvenile fish with Aeromonas hydrophila
Dietary myo-inositol modulates immunity through antioxidant activity and the Nrf2 and E2F4/cyclin signalling factors in the head kidney and spleen following infection of juvenile fish with Aeromonas hydrophila
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幼鱼感染嗜水气单胞菌后，膳食肌醇通过抗氧化活性以及头肾和脾脏中的 Nrf2 和 E2F4/细胞周期蛋白信号因子调节免疫力
DOI：
10.1016/j.fsi.2015.12.017
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发表时间：
2016-02-01
影响因子：
4.7
通讯作者：
Feng, Lin
中科院分区：
文献类型：
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作者：
Jiang, Wei-Dan;Hu, Kai;Feng, Lin
本研究旨在探讨饲料中添加维生素肌醇（MI）对鱼类感染主要淡水病原菌嗜水气单胞菌后头肾和脾脏的免疫力和结构完整性的影响。结果首次表明，与适宜MI水平相比，MI缺乏降低了头肾和脾脏中溶菌酶和酸性磷酸酶（ACP）活性以及补体C3和C4含量，表明MI缺乏降低了这些重要免疫器官的免疫力。MI缺乏导致的免疫抑制部分与氧化损伤有关[表现为丙二醛（MDA）和蛋白质羰基（PC）含量的增加]，而氧化损伤又部分归因于谷胱甘肽（GSH）含量的降低和抗氧化酶活性[总超氧化物歧化酶（T-SOD）、CuZnSOD、MnSOD、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GPx）和谷胱甘肽还原酶（GR）]。MI缺乏抑制了A.你好由于MI缺乏引起的氧化损伤也导致增殖相关信号传导（细胞周期蛋白D1、细胞周期蛋白A、细胞周期蛋白E和E2 F4）的抑制。因此，MI缺乏部分抑制损伤修复。过量的MI表现出类似于MI不足的负面影响，而最佳MI含量逆转了这些指标。这些观察结果表明，MI缺乏或过量可导致免疫系统的抑制，这可能部分与氧化损伤、抗氧化紊乱以及在鱼感染A.你好幼建鲤头肾和脾脏的适宜MI水平分别为660.7（以ACP计）和736.8 mg kg（-1）（以MDA计），770.5（以ACP计）和766.9 mg kg（-1）（以MDA计）。(C)2015爱思唯尔有限公司版权所有。
This study was conducted to investigate the effects of the dietary vitamin myo-inositol (MI), on the immunity and structural integrity of the head kidney and spleen following infection of fish with the major freshwater pathogen bacterial Aeromonas hydrophila. The results demonstrated for the first time that MI deficiency depressed the lysozyme and acid phosphatase (ACP) activities and the complement 3 (C3) and C4 contents in the head kidney and spleen compared with the optimal MI levels, indicating that MI deficiency decreased the immunity of these important fish immune organs. The depression in immunity due to MI deficiency was partially related to oxidative damage [indicated by increases in the malondialdehyde (MDA) and protein carbonyl (PC) contents] that was in turn partially due to the decreased glutathione (GSH) content and the disturbances in antioxidant enzyme activities [total superoxide dismutase (T-SOD), CuZnSOD, MnSOD, catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR)]. MI deficiency inhibited the antioxidant-related gene transcription [CuZnSOD, MnSOD, CAT, GPx1a, GR and NF-E2-related factor 2 (Nrf2)] in the head kidney and spleen following infection of the fish with A. hydrophila. The oxidative damage due to MI deficiency also resulted in the inhibition of proliferation-associated signalling (cyclin D1, cyclin A, cyclin E and E2F4). Thus, MI deficiency partially inhibited damage repair. Excessive MI exhibited negative effects that were similar to MI deficiency, whereas the optimal MI content reversed those indicators. These observations indicated that an MI deficiency or excess could cause depression of the immune system that might be partially related to oxidative damage, antioxidant disturbances, and the inhibition of the proliferation-associated signalling in the head kidney and spleen following infection of fish with A. hydrophila. Finally, the optimal MI levels were 660.7 (based on ACP) and 736.8 mg kg(-1) diet (based on MDA) in the head kidney and 770.5 (based on ACP) and 766.9 mg kg(-1) diet (based on MDA) in the spleen of juvenile Jian carp. (C) 2015 Elsevier Ltd. All rights reserved.