Selenium-enriched Bacillus paralicheniformis SR14 attenuates H2O2-induced oxidative damage in porcine jejunum epithelial cells via the MAPK pathway.

Oxidative stress plays a detrimental role in gastrointestinal disorders. Although selenium-enriched probiotics have been shown to strengthen oxidation resistance and innate immunity, the potential mechanism remains unclear. Here, we focused on the biological function of our material, selenium-enriched Bacillus paralicheniformis SR14 (Se-BP), and investigated the antioxidative effects of Se-BP and its underlying molecular mechanism in porcine jejunum epithelial cells. First, we prepared Se-BP and quantified for its selenium and bacterial contents. Then, in vitro free radical scavenging activity was measured to evaluate the potential antioxidant effect of Se-BP. Third, to induce an appropriate oxidative stress model, we adopted different concentrations of H2O2 and determined the most suitable concentration by a methyl thiazolyl tetrazolium (MTT) assay. Regarding treatment with Se-BP and H2O2, we found that Se-BP increased cell viability and prevented lactate dehydrogenase release when administered prior to H2O2 exposure. Additionally, Se-BP markedly suppressed reactive oxygen species and malondialdehyde production in cells and effectively attenuated apoptosis. Compared with incubation with H2O2 alone, treatment with Se-BP significantly promoted phosphorylation of ERK and p38 MAPK signaling molecules. When administered with ERK and p38 MAPK inhibitors, Se-BP did not alleviate the decrease in cell viability. Our results suggest that Se-BP prevents H2O2-induced cell damage by activating the ERK/p38 MAPK signaling pathways.