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首页> 外文期刊>Cancer prevention research. >Soy Protein Isolate Protects Against Ethanol-Mediated Tumor Progression in Diethylnitrosamine-Treated Male Mice
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Soy Protein Isolate Protects Against Ethanol-Mediated Tumor Progression in Diethylnitrosamine-Treated Male Mice

机译：大豆分离蛋白可防止乙醇介导的二乙基亚硝胺处理的雄性小鼠肿瘤的进展。

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In this study, diethylnitrosamine-treated male mice were assigned to three groups: (i) a 35% high fat ethanol liquid diet (EtOH) with casein as the protein source, (ii) the same EtOH liquid diet with soy protein isolate as the sole protein source (EtOH/SPI), (iii) and a chow group. EtOH feeding continued for 16 weeks. As expected, EtOH increased the incidence and multiplicity of basophilic lesions and adenomas compared with the chow group, P < 0.05. Soy protein replacement of casein in the EtOH diet significantly reduced adenoma progression when compared with the EtOH and EtOH/SPI group (P < 0.05). Tumor reduction in the EtOH/SPI group corresponded to reduced liver injury associated with decreased hepatic Tnfa and Cd14 antigen (Cd14) expression and decreased nuclear accumulation of NF-kappa B1 protein compared with the EtOH group (P < 0.05). Detection of sphingolipids using high-resolution matrix-assisted laser desorption/ionization-Fourier transform ion cyclotron resonance (MALDI-FTICR) imaging mass spectrometry revealed increased accumulation of long acyl chain ceramide species, and sphingosine-1-phosphate (S1P) in the EtOH group that were significantly reduced in the EtOH/SPI group. Chronic EtOH feeding also increased mRNA expression of beta-catenin transcriptional targets, including cyclin D1 (Ccnd1), matrix metallopeptidase 7 (Mmp7), and glutamine synthetase (Glns), which were reduced in the EtOH/SPI group (P < 0.05). We conclude that soy prevents tumorigenesis by reducing proinflammatory and oxidative environment resulting from EtOH-induced hepatic injury, and by reducing hepatocyte proliferation through inhibition of b-catenin signaling. These mechanisms may involve changes in sphingolipid signaling. (C) 2016 AACR.
机译：在这项研究中，将经二乙基亚硝胺处理的雄性小鼠分为三组：（i）以酪蛋白为蛋白质源的35％高脂乙醇流质饮食（EtOH），（ii）与大豆蛋白分离物相同的EtOH流质饮食与大豆分离蛋白唯一的蛋白质来源（EtOH / SPI），（iii）和一个食物团。乙醇喂养持续了16周。正如预期的那样，与食物组相比，EtOH增加了嗜碱性病变和腺瘤的发生率和多样性，P <0.05。与EtOH和EtOH / SPI组相比，EtOH饮食中酪蛋白的大豆蛋白替代显着降低了腺瘤的进展（P <0.05）。与EtOH组相比，EtOH / SPI组的肿瘤减少对应于与肝Tnfa和Cd14抗原（Cd14）表达降低以及NF-κB1蛋白的核蓄积减少相关的肝损伤的减轻（P <0.05）。使用高分辨率基质辅助激光解吸/电离-傅立叶变换离子回旋共振（MALDI-FTICR）成像质谱检测鞘脂，发现长酰基链神经酰胺物质积累增加，并且EtOH中的鞘氨醇-1-磷酸（S1P）增加EtOH / SPI组明显降低。长期饲喂EtOH还增加了β-catenin转录靶标的mRNA表达，包括cyclin D1（Ccnd1），基质金属肽酶7（Mmp7）和谷氨酰胺合成酶（Glns），这些在EtOH / SPI组中均降低（P <0.05）。我们得出的结论是，大豆可通过减少EtOH诱导的肝损伤导致的促炎和氧化环境，以及通过抑制b-catenin信号传导来减少肝细胞增殖来预防肿瘤发生。这些机制可能涉及鞘脂信号传导的变化。 （C）2016 AACR。

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