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Roles of JNK, ERK, and PI3K/AKT signaling pathways in zinc-mediated alleviation of thermal stress-induced damage to the integrity and barrier function of primary cultured chick jejunal epithelial cells

文献类型： 外文期刊

作者： Liang Huang;Chunyu Cao;Xuanxu Lin;Wei Wu;Xi Lin;Hsiao Ching Liu;Jack Odle;Miles Todd See;Liyang Zhang;Lin Lu;Xugang Luo;Xiudong Liao

作者机构：

关键词： integrity and barrier function;jejunal epithelial cell;signaling pathway;thermal stress;zinc

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： This study investigated the precise alleviating mechanisms of Zn on chick embryonic jejunal epithelial cells under thermal stress (TS) and elucidated signaling pathways directly involved in this process. Experiment 1 identified the effective concentrations of inhibitors or agonists for extracellular regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), and phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT). The data were analyzed using one-way ANOVA. In experiment 2, a randomized factorial design consisting of 3 controls + 3 cell types × 3 Zn treatments was used to confirm the effect of Zn and cell type on each signaling pathway. Under heat stress (HT, 44°C), 3 cell types in which the signaling pathways were normal, inhibited, or overexpressed were subjected to 3 treatments consisting of supplementation with inorganic Zn sulfate (iZn), organic Zn proteinate (oZn), or no Zn supplementation (containing 3.98 μmol Zn/L). Under normal temperature (NT, 40 °C), the 3 cell types without Zn addition as controls. The significant differences between NT and HT across each cell type were conducted by T-test, data under HT were evaluated using two-way ANOVA. The results showed that TS decreased transepithelial resistance (TEER), claudin-1 and zona occludens-1 (ZO-1) mRNA levels, phosphorylated (p)-ERK/ERK, p-PI3K/PI3K, and p-AKT/AKT levels, and increased phenol red permeability compared with NT in 3 cell types (P < 0.05). Under HT, iZn and oZn decreased phenol red permeability and diamine oxidase (DAO), while increasing cell proliferation, claudin-1, occludin, and junctional adhesion molecule-A (JAM-A) mRNA and p-ERK/ERK level in normal cells, and the above mRNA levels were higher in the oZn group than in the iZn group (P < 0.05); however, different Zn treatments had no effect on DAO and cell proliferation in ERK inhibited and overexpression cells (P > 0.05). The interaction between cell type and Zn treatment did not affect the integrity and barrier function indices and p-JNK/JNK level in the cells for the JNK signaling pathway (P > 0.05). Supplemental iZn and oZn increased TEER, cell proliferation, claudin-1 and p-PI3K/PI3K level in normal cells (P < 0.05), but different Zn treatments had no effect on phenol red permeability, DAO and cell proliferation in PI3K/AKT inhibited and over expression cells, and ZO-1 mRNA and protein levels and p-PI3K/PI3K level in over expression cells (P > 0.05). Therefore, the above results show that Zn could alleviate TS-induced damage to the integrity and barrier function of chick embryonic jejunal epithelial cells via the ERK and PI3K/AKT signaling pathways.

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