Saccharomyces Boulardii Exerts Anti-Apoptosis And Anti-Necroptosis Effects On Neonatal Mice Necrotizing Enterocolitis By Increasing Reactive Oxygen Species Consumption

Oxidative stress and exaggerated inflammatory response play crucial roles in necrotizing enterocolitis (NEC). Although Saccharomyces boulardii (S. boulardii) participates in many different biological activities, it remains unknown whether S. boulardii inhibits cell death induced by NEC. Furthermore, mechanisms against oxidative stress levels have not yet been elucidated. The present study established an experimental mouse model of NEC obtained after artificial feeding + hypoxia/re-oxygenation cooling stimulation + lipopolysaccharide for 3 days. Hematoxylin and eosin (HE) staining and morphologic studies were performed to define the model. After S. boulardii treatment, weights and survivor numbers were significantly increased, while intestinal tissue damage was reduced. Necroptosis and apoptosis were inhibited by S. boulardii. Protein and mRNA expression levels of caspase-3, caspase-8, and RIP3 further confirmed the protection of S. boulardii. Furthermore, S. boulardii increased super oxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) levels, while promoting clearing of reactive oxygen species (ROS) and malondialdehyde (M DA). The current study provides the first evidence that S. boulardii exerts anti-apoptosis and necroptosis effects in NEC intestinal tissues through increasing ROS consumption.