新生期缺氧对小鼠肠道的损伤作用及机制研究OA

To reveal the pathological basis of neonatal hypoxic enteropathy,this study used newborn mice as a model to investigate the damaging effects of hypoxia on intestinal tissue during the neonatal period and the underlying mechanisms from both morphological and molecular perspectives.The results showed that hypoxia led to a significant decrease in body weight of neonatal mice.Hematoxylin and eosin(HE)staining results indicated that hypoxia caused developmental abnormalities in the ileum and distal colon of mice,manifested as necrosis of intestinal epithelial cells,inflammatory cell infiltration,and damage to the mucosal barrier.The Stress&Toxicity Pathway Finder PCR revealed that hypoxia broadly perturbed multiple key molecular pathways.The expression of the oxidative stress-related gene Sod1 was downregulated,while the expression of Ldha(involved in energy metabolism reprogramming),the water channel protein Aqp4,the key pyroptosis molecule Caspase-1,the necroptosis molecule Ripk3,and the inflammatory signaling molecules Ccl12,Mmp9,and Tlr4 were all significantly upregulated.Additionally,the expression of the autophagy-related gene Atg7 was inhibited.These findings suggest that neonatal hypoxia may mediate intestinal structural and functional damage through multiple mechanisms,including oxidative stress imbalance,energy metabolism dysregulation,programmed cell death,inflammatory responses,and autophagy inhibition.