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.

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.

Relative bioavailability of selenium yeast, selenomethionine, hydroxyl-selenomethionine and nano-selenium for broilers.

Selenium (Se) is an essential trace element for humans and animals. Development and application of new forms of Se sources with lower toxicity and higher bioavailability has been attracting more attention. However, the bioavailabilities of Se from several new Se sources for broilers remain unclear.

Zinc alleviates thermal stress-induced damage to the integrity and barrier function of cultured chicken embryonic primary jejunal epithelial cells via the MAPK and PI3K/AKT/mTOR signaling pathways.

Zinc (Zn) could alleviate the adverse effect of high temperature (HT) on intestinal integrity and barrier function of broilers, but the underlying mechanisms remain unclear. We aimed to investigate the possible protective mechanisms of Zn on primary cultured broiler jejunal epithelial cells exposed to thermal stress (TS). In Exp.