数字农科院2.0

Zinc proteinate alleviates thermal stress-induced damage to broiler jejunal organoid integrity and barrier function possibly by promoting cell proliferation via GPR39/PLCβ1-mediated PI3K/AKT and MAPK signaling pathways

文献类型： 外文期刊

作者： Weizhen Song;Yangyang Hu;Weiyun Zhang;Xi Lin;Hsiao Ching Liu;Jack Odle;Miles Todd See;Yun Hu;Tingting Li;Shengchen Wang;Xiaoyan Cui;Xiudong Liao;Liyang Zhang;Xugang Luo

作者机构：

关键词： broiler jejunal organoids;cell proliferation;G protein-coupled receptor 39 / phospholipase C beta 1-mediated phosphatidylinositol 3-kinase / serine threonine kinase and mitogen activated protein kinase signaling pathways;integrity and barrier function;thermal stress;zinc proteinate with moderate chelation strength

期刊名称： Journal of Animal Science

ISSN： 0021-8812

年卷期： 2025 年 103 卷

页码：

收录情况： SCIE（2025版）

摘要： No study is currently available regarding the establishment and utilization of a thermal stress (TS)-induced damage model in animal intestinal organoids (IO). To study the efficacy and possible molecular mechanisms of zinc (Zn) proteinate with moderate chelation strength (Zn-Prot M) in alleviating TS-induced intestinal damage, two experiments were conducted by establishing and using the TS-induced damage model of broiler jejunal organoids (JO). In Exp. 1, the effect of TS on the integrity and barrier function of JOs over time was investigated using a 2 [culture temperatures, 40°C (normal temperature, NT) and 44°C (high temperature, HT)] × 6 (incubation time points, 0, 3, 6, 9, 12, and 15 h) factorial design, and the data were analyzed by single degree of freedom contrast and two-way ANOVA. In Exp. 2, the efficacies of Zn-Prot M and Zn sulfate (ZnS) in reducing the effect of TS were compared via 2 (Zn sources, ZnS and Zn-Prot M) × 2 (added Zn levels, 50 and 100 μmol/L) factorial design with control groups under HT (HT-C) and NT (NT-C), and the data were analyzed by T-test, single degree of freedom contrast and two-way ANOVA. The results showed that in Exp. 1, the integrity and barrier function of JOs were substantially damaged after 12 h of TS, as evidenced by the increased diamine oxidase (DAO) content by 17% and lactate dehydrogenase (LDH) activity by 84% (P < 0.05) and the observed fluorescein isothiocyanate-dextran (FITC-D) entrance into the JOs. In Exp. 2, TS increased (P < 0.05) DAO contents by 95% and LDH activities by 105% in the culture media, and mRNA or phosphorylated protein expression levels of C-jun N-terminal kinase (JNK) by 27% or 117%, and FITC-D accumulation was observed in the JOs. TS decreased (P < 0.05) the budding percentage of JOs by 35% and proportions of proliferating cell nuclear antigen (PCNA) by 56% and 5-ethynyl-2'-deoxyuridine (EdU) positive cells by 58%. Additionally, TS decreased (P < 0.05) mRNA and protein or phosphorylated protein expression levels of G protein-coupled receptor 39 (GPR39), phospholipase C beta 1 (PLCβ1), phosphatidylinositol 3-kinase (PI3K), serine threonine kinase (AKT), extracellular regulated protein kinase (ERK), and p38 mitogen activated protein kinase (p38 MAPK) by 37-72%. Meanwhile, supplementation of Zn, particularly 50 μmol/L of Zn as Zn-Prot M, reversed (P < 0.05) all the above changes by 21-132%. In conclusion, supplemental Zn, particularly 50 μmol/L of Zn as Zn-Prot M, could effectively alleviate the TS-induced damage to the integrity and barrier function of broiler JOs possibly by promoting cell proliferation via GPR39/PLCβ1-mediated PI3K/AKT and MAPK signaling pathways. To our knowledge, this is the first study to establish and utilize the TS-induced damage model in animal IOs to explore the protective efficacy of a nutrient and possible mechanisms.

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