DOI: 10.57760/sciencedb.zhwcyxzz.01043
title: The Regulatory Role of Autophagy in Intestinal Inflammation and Epithelial Barrier Function in NEC Rats
title: 细胞自噬对NEC大鼠肠道炎症及上皮屏障功能的调控作用

description: Objective To investigate the mechanism of autophagy in a neonatal rat model of necrotizing enterocolitis (NEC). Methods Forty-five neonatal Sprague-Dawley (SD) rats were randomly divided into three groups: the NEC model group, the autophagy-inhibited NEC group, and the autophagy-induced NEC group. The clinical manifestations of rats were compared among the three groups. Intestinal pathology was observed under an electron microscope. 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 &lt; 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 &lt; 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.
description: Objective To investigate the mechanism of autophagy in a neonatal rat model of necrotizing enterocolitis (NEC). Methods Forty-five neonatal Sprague-Dawley (SD) rats were randomly divided into three groups: the NEC model group, the autophagy-inhibited NEC group, and the autophagy-induced NEC group. The clinical manifestations of rats were compared among the three groups. Intestinal pathology was observed under an electron microscope. 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 &lt; 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 &lt; 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.