Fish Skin Gelatin Hydrolysate Production by Ginger Powder Induces Glutathione Synthesis To Prevent Hydrogen Peroxide Induced Intestinal Oxidative Stress via the Pept1-p62-Nrf2 Cascade,Journal of Agricultural and Food Chemistry

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Fish Skin Gelatin Hydrolysate Production by Ginger Powder Induces Glutathione Synthesis To Prevent Hydrogen Peroxide Induced Intestinal Oxidative Stress via the Pept1-p62-Nrf2 Cascade
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2018-10-19 00:00:00 , DOI: 10.1021/acs.jafc.8b02840
Liufeng Zheng _{1,

2} , Hongkui Wei _{1,

3} , Huichao Yu ₁ , Qian Xing ₂ , Yi Zou ₁ , Yuanfei Zhou _{1,

3} , Jian Peng _{1,

3}

Affiliation

Gelatin hydrolysate was reported to contain large amounts of biologically active peptides with excellent antioxidant properties. However, its inducement of antioxidant response within cells and the underlying molecular mechanism are far from clear. Here, gelatin from Nile tilapia skin was hydrolyzed by ginger protease to produce antioxidant hydrolysate, and three fish skin gelatin hydrolysate fractions (FSGHFs) were obtained by ultrafiltration. Fractionation of the hydrolysate increased the free radical scavenging capacity of the FSGHFs, particularly FSGHF3, which showed the lowest molecular weight (below 1000 Da). Furthermore, FSGHF3 treatment prior to H₂O₂ exposure increased cell viability and membrane integrity in IPEC-J2 cells. H₂O₂-induced ROS production and epithelial barrier damage were suppressed by FSGHF3 pretreatment. FSGHF3 stimulated the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2), along with increases in the mRNA and protein expression of catalytic and modulatory subunits of γ-glutamylcysteine ligase as well as in the level of glutathione. Silencing of Nrf2 or p62 (an upstream regulator of Nrf2) suppressed FSGHF3-induced Nrf2 activation and its protection against H₂O₂-induced oxidative stress. Moreover, oligopeptides in FSGHF3 may mediate the cytoprotective effect against oxidative stress, which was confirmed by the result that FSGHF3 failed to inhibit the ROS production in H₂O₂-exposed cells with the knockdown of Pept1 (an oligopeptide transporter). Therefore, FSGHF3 can induce glutathione synthesis and prevent oxidative stress through the Pept1-p62-Nrf2 cascade and thus may be a functional food for gastrointestinal dysfunction.

中文翻译：

生姜粉生产鱼皮明胶水解物诱导谷胱甘肽合成，通过 Pept1-p62-Nrf2 级联防止过氧化氢诱导的肠道氧化应激

据报道，明胶水解物含有大量具有优异抗氧化特性的生物活性肽。然而，它在细胞内诱导抗氧化反应及其潜在的分子机制尚不清楚。本研究利用生姜蛋白酶水解尼罗罗非鱼皮中的明胶，产生抗氧化水解液，并通过超滤获得三种鱼皮明胶水解液组分（FSGHF）。水解产物的分级提高了 FSGHF 的自由基清除能力，特别是 FSGHF3，其分子量最低（低于 1000 Da）。此外，H ₂ O ₂暴露之前的 FSGHF3 处理增加了 IPEC-J2 细胞的细胞活力和膜完整性。 FSGHF3 预处理抑制了 H ₂ O ₂诱导的 ROS 产生和上皮屏障损伤。 FSGHF3 刺激核因子红细胞 2 相关因子 2 (Nrf2) 的核转位，同时增加 γ-谷氨酰半胱氨酸连接酶催化和调节亚基的 mRNA 和蛋白质表达以及谷胱甘肽水平。 Nrf2 或 p62（Nrf2 的上游调节因子）的沉默抑制了 FSGHF3 诱导的 Nrf2 激活及其对 H ₂ O ₂诱导的氧化应激的保护。此外，FSGHF3中的寡肽可能介导针对氧化应激的细胞保护作用，通过敲低Pept1（寡肽转运蛋白），FSGHF3未能抑制暴露于H ₂ O ₂的细胞中ROS产生的结果证实了这一点。因此，FSGHF3可以通过Pept1-p62-Nrf2级联诱导谷胱甘肽合成并防止氧化应激，因此可能成为胃肠功能障碍的功能性食品。

更新日期：2018-10-19

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