关键词: 放射性肠损伤, 寡糖类, 炎症因子

Abstract: Objective To explore the protective mechanism of human milk oligosaccharides (HMOs) on radiation-induced intestinal injury (RIII). 
Methods A mouse model of RIII was constructed and treated with HMOs by gavage. HE staining was used to detect the intestinal villus length and crypt depth of mice. Spectrophotometry was used to detect the changes of serum D-lactic acid and D-xylose in mice to determine intestinal permeability, and myeloperoxidase(MPO) activity kit was used to detect neutrophil infiltration in intestinal tissue. Enzyme-linked immunosorbent assay kit was used to detect the changes of inflammatory factors in intestinal tissue, and qRT-PCR was used to detect the expression level of TLR4 mRNA in intestinal tissue. 
Results Compared with the IR group, the IR+HMOs group prompted a significant increase in epithelial thickness (413.208±37.042)μm and crypt number (65.109±8.225) (P＜0.05), a significant decrease in serum D-lactic acid level (1.799±0.158)μg/L, and a significant increase in D-xylose level (76.823±12.206) mg/L (P＜0.05). Moreover, in the IR+HMOs group, the levels of tumor necrosis factor-α (TNF-α) (42.000±5.858)ng/L and interleukin-1β (IL-1β) (38.836±4.022) ng/L in the intestinal tissues of mice, and the infiltration of neutrophils (4.024±0.419) U/L were significantly decreased, while the level of anti-inflammatory factor interleukin-10 (IL-10) (24.392±2.989) ng/L was increased significantly. In addition, TLR4 expression in the intestinal tissues of mice in the IR group (3.22±0.53) was increased compared with that in the Sham group (1.00±0.09), whereas the expression level of TLR4 mRNA was significantly higher in the IR+HMOs group than that in the IR group. 
Conclusion HMOs-mediated TLR4 plays a protective role in RIII. 

Key words: radiation-induced intestinal injury, oligosaccharides, inflammatory factors