Effect of Endoplasmic Reticulum Stress-induced Autophagy on Necrotizing Enterocolitis in Neonatal Rats
10.11969/j.issn.1673-548X.2024.02.021
- VernacularTitle:内质网应激诱导的自噬对新生大鼠坏死性小肠结肠炎的影响
- Author:
Lihong WANG
1
;
Xiaoli YANG
;
Jing LI
Author Information
1. 030000 太原,山西医科大学儿科医学系
- Keywords:
Endoplasmic reticulum stress;
Autophagy;
Necrotizing enterocolitis;
Intestinal epithelial cells;
Mechanism of action
- From:
Journal of Medical Research
2024;53(2):106-111
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of inhibiting autophagy induced by endoplasmic reticulum stress(ERS)on necrotiz-ing enterocolitis(NEC)in neonatal rats.Methods First,the NEC model of neonatal rats was established.Then,the intestinal epitheli-al cells were isolated and divided into three groups:control group,inhibition group and induction group.The control group was cultured normally,the inhibition group was added with 4-phenylbutyric acid,and the induction group was added with tunicamycin for 24hours.Enzyme-linked immunosorbent assay(ELISA)was used to detect the expression of the cellular inflammatory cytokines tumor necrosis factor-α(TNF-α)and intestinal fatty acid binding protein(I-FABP)in each group.Real-time quantitative polymerase chain reac-tion(RT-qPCR)was used to detect the mRNA expression level of the markers of ERS glucose regulated protein 78(GRP78)and oxy-gen-regulated protein 150(ORP150).Western blot was used to detect the expression of autophagy related proteins LC3 Ⅱ/Ⅰ and p62.Results Compared with the control group,the expression of p62 in the inhibition group increased significantly,the expression of TNF-α,I-FABP,GRP78,ORP150,LC3 Ⅱ/Ⅰ in the inhibition group was significantly decreased,while the expression of p62 in the induc-tion group was significantly decreased,the expressions of TNF-α,Ⅰ-FABP,GRP78,ORP150,LC3 Ⅱ/Ⅰ were significantly increased,and the differences were statistically significant(P＜0.05).Conclusion Inhibition of ERS induced autophagy activation can alleviate intestinal mucosal injury and inflammatory response in neonatal rats with NEC and improve intestinal barrier function.
