Biogenic Nano-Selenium Particles Effectively Attenuate Oxidative Stress-Induced Intestinal Epithelial Barrier Injury By Activating the Nrf2 Antioxidant Pathway

Oxidative stress has been implicated in a wide range of animal diseases. Due to frequent enterocyte renewal and continuous exposure to exogenous agents, the intestine is more vulnerable to oxidative stress than other organs which lead to intestinal inflammation, barrier injury and dysfunction, and finally decrease animal production efficiency. In the present study, a new form of selenium nanoparticle (biogenic nano-selenium (BNS) particles) was synthesized using bacteria. The protection of BNS particles against oxidative stress-induced intestinal barrier dysfunction and the inherent mechanisms of this process were investigated, and selenomethionine (SeMet) and chemically synthesized nano-selenium (Nano-Se) particles were used for comparison. Characterization of BNS particles revealed that they were monodisperse and homogeneous spheres with an average size of 139.43 ± 7.44 nm. In the mouse model of intestinal oxidative stress, BNS particles were found to protect the mouse intestinal barrier function and preserve intestinal redox homeostasis more efficiently than SeMet and Nano-Se. In vitro experiments with porcine jejunum epithelial (IPEC-J2) cells verified the stronger epithelial barrier-protecting effect of BNS particles against oxidative stress with reduced cell apoptosis and an improved cell redox state. BNS activated nuclear factor (erythroid-derived-2)-like 2 (Nrf2) and increased the expression of its downstream genes, including thioredoxin reductase (TXNRD)-1, NADPH dehydrogenase (NQO)-1, heme oxygenase (HO)-1 and thioredoxin (Trx), in dose- and time-dependent manners. In contrast, SeMet and Nano-Se merely enhanced the activity of the selenoenzymes TXNRD-1 and glutathione peroxidase (GPx)-1, indicating the role of selenium donors. Moreover, knockdown of Nrf2 significantly blocked the antioxidative effect of BNS, confirming that BNS protects the intestinal barrier from oxidative stress-induced damage by activating Nrf2 and its downstream genes. Our results suggest that BNS is a promising selenium species with potential application in treating oxidative stress related intestinal diseases.