The Regulatory Role of Autophagy in Intestinal Inflammation and Epithelial Barrier Function in NEC Rats

Immunohistochemistry (IHC) was used to detect the expression of ZO-1 in the ileal tissue. Enzyme-linked immunosorbent assay (ELISA) was employed to measure the levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in intestinal tissues. Western blotting was used to detect the expression levels of autophagy-related proteins p62 and microtubule-associated protein 1 light chain 3 (LC3) Ⅱ and Ⅰ, and the LC3Ⅱ/Ⅰ ratio was calculated.

One-way analysis of variance (ANOVA) was used for statistical analysis of the above results, and the least significant difference (LSD) test was used for further pairwise comparisons. Results The clinical manifestation score, pathological score, IL-6 and TNF-α levels, and LC3Ⅱ/Ⅰ ratio in the autophagy-induced group were significantly higher than those in the NEC group and autophagy-inhibited group, and those in the NEC group were significantly higher than those in the autophagy-inhibited group； all differences were statistically significant (P < 0.05).

The ZO-1 level and p62 expression in the autophagy-induced group were significantly lower than those in the NEC group and autophagy-inhibited group, and those in the NEC group were significantly lower than those in the autophagy-inhibited group；all differences were statistically significant (P < 0.05). Conclusion Autophagy in epithelial cells can regulate the occurrence of NEC by modulating inflammatory responses and intestinal mucosal epithelial barrier function, and inhibiting intestinal epithelial cell autophagy can alleviate the clinical symptoms of NEC.