Zinc glycine chelate (Zn-Gly) has anti-inflammation and growth-promoting properties; however, the mechanism of Zn-Gly contribution to gut barrier function in Cherry Valley ducks during intestinal inflammation is unknown. Three-hundred 1-day-old ducks were divided into 5 groups (6 replicates and 10 ducks per replicate) in a completely randomized design: the control and dextran sulfate sodium (DSS) groups were fed a corn-soybean meal basal diet, and experimental groups received supplements of 70, 120 or 170 mg/kg Zn in form of Zn-Gly. The DSS and treatment groups were given 2 mL of 0.45 g/mL DSS daily during d 15–21, and the control group received normal saline. The experiment lasted 21 d. Compared with DSS group, 70, 120 and 170 mg/kg Zn significantly increased body weight (BW), villus height and the ratio of villus to crypt, and significantly decreased the crypt depth of jejunum at 21 d. The number of goblet cells in jejunal villi in the Zn-Gly group was significantly increased by periodic acid-Schiff staining. Compared with control, the content of intestinal permeability marker D-lactic acid (D-LA) and fluxes of fluorescein isothiocyanate (FITC-D) in plasma of DSS group significantly increased, and 170 mg/kg Zn supplementation significantly decreased the D-LA content and FITC-D fluxes. Compared with control, contents of plasma, jejunum endotoxin and jejunum pro-inflammatory factors IL-1β, IL-6 and TNF-α were significantly increased in DSS group, and were significantly decreased by 170 mg/kg Zn supplementation. Dietary Zn significantly increased the contents of anti-inflammatory factors IL-10, IL-22 and sIgA and IgG in jejunum. Real-time PCR and Western blot results showed that 170 mg/kg Zn supplementation significantly increased mRNA expression levels of CLDN-1 and expression of OCLN protein in jejunum, and decreased gene and protein expression of CLDN-2 compared with DSS group. The 120 mg/kg Zn significantly promoted the expressions of IL-22 and IgA. Dietary Zn-Gly supplementation significantly decreased pro-inflammatory genes IL-8 and TNF-α expression levels and TNF-α protein expression in jejunum. Additionally, Zn significantly reduced the gene and protein expression of TLR4, MYD88 and NF-κB p65. Zn-Gly improved duck BW and alleviated intestinal injury by regulating intestinal morphology, barrier function and gut inflammation-related signal pathways TLR4/MYD88/NF-κB p65.

中文翻译：

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甘氨酸锌螯合物通过减弱 TLR4/NF-κB 通路改善 DSS 诱导的肉鸭肠道屏障功能障碍

甘氨酸锌螯合物（Zn-Gly）具有抗炎和促进生长的特性；然而，Zn-Gly 在肠道炎症期间对樱桃谷鸭肠道屏障功能的贡献机制尚不清楚。采用完全随机设计，将 300 只 1 日龄鸭分为 5 组（6 个重复，每个重复 10 只鸭）：对照组和葡聚糖硫酸钠 (DSS) 组饲喂玉米-豆粕基础日粮，实验组接受 70、120 或 170 mg/kg Zn-Gly 形式的锌补充剂。DSS 组和治疗组在第 15-21 天期间每天给予 2 mL 0.45 g/mL DSS，对照组接受生理盐水。实验持续21 d。与DSS组相比，70、120和170 mg/kg Zn在21 d时显着增加了体重（BW）、绒毛高度和绒毛与隐窝的比率，并显着降低了空肠隐窝深度。高碘酸希夫染色显示 Zn-Gly 组空肠绒毛中杯状细胞的数量显着增加。与对照组相比，DSS组血浆中肠道通透性标志物D-乳酸（D-LA）含量和异硫氰酸荧光素（FITC-D）通量显着升高，补锌170 mg/kg显着降低D-LA含量和 FITC-D 通量。与对照组相比，DSS组血浆、空肠内毒素和空肠促炎因子IL-1β、IL-6和TNF-α的含量显着升高，而补充170 mg/kg Zn则显着降低。膳食锌显着增加空肠中抗炎因子IL-10、IL-22以及sIgA和IgG的含量。实时PCR和Western blot结果显示，与DSS组相比，170 mg/kg Zn补充显着增加了空肠中CLDN-1 mRNA表达水平和OCLN蛋白表达，并降低了CLDN-2基因和蛋白表达。120 mg/kg Zn显着促进IL-22和IgA的表达。膳食中补充 Zn-Gly 可显着降低空肠中促炎基因 IL-8 和 TNF-α 的表达水平以及 TNF-α 蛋白的表达。此外，Zn 显着降低了 TLR4、MYD88 和 NF-κB p65 的基因和蛋白表达。Zn-Gly通过调节肠道形态、屏障功能和肠道炎症相关信号通路TLR4/MYD88/NF-κB p65来改善鸭体重并减轻肠道损伤。