Selenomethionine combined with allicin delays reactive oxidative stress-induced apoptosis, inflammation, endoplasmic reticulum stress, and barrier damage in IPEC-J2 cells via the GPX4 signaling pathway

Abstract

To increase livestock productivity and improve economic efficiency, farms tend to focus on the growth rate of livestock and poultry. This strategy can result in a reduced resistance to reactive oxidative stress (ROS) and heat stress. Selenomethionine (SeMet) and allicin have antioxidant properties, but their excessive intake can lead to toxicity. Co-administration improves antioxidant protection and reduces side-effects but also reduces the cost of administration. We undertook a study to elucidate the antioxidant effect of glutathione peroxidase (GPX) 4 in SeMet and allicin. The synergistic antioxidant effect, attenuation of endoplasmic reticulum stress (ERS), enhancement of expression of tight-junction proteins, and inhibition of apoptosis, ferroptosis, inflammatory responses of SeMet and allicin were attenuated significantly after inhibition of GPX4 according to western blotting (P < 0.05). These results indicated that activation of the GPX4 pathway was the key to the synergistic maintenance of barrier function, attenuation of ERS, as well as inhibition of apoptosis, ferroptosis, and inflammatory responses by SeMet and allicin. SeMet and allicin could protect the intestinal barrier from oxidative damage by synergistically activating the GPX4 pathway, increasing antioxidant capacity, and improving growth performance. In conclusion, SeMet and allicin could be used as a new drug combination to alleviate diseases associated with intestinal ROS and aid in the development of new antioxidant feed additives.