EGF enema and EGFR monoclonal antibody injection alleviate the inflammatory bowel disease in AMO/DSS induced mice model
Xueyan Zheng
Orcid profile and Chengdang Wang
Orcid profile 
Article Category: Original Study
Published Online: Jun 21, 2025
Page range: 87 - 94
Received: Sep 19, 2024
Accepted: May 12, 2025
DOI: https://doi.org/10.2478/ahem-2025-0011
Keywords
© 2025 Xueyan Zheng et al., published by Sciendo
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
Introduction
Inflammatory bowel disease (IBD) is a chronic condition that significantly impacts the gastrointestinal system. Using an AMO/DSS-induced IBD mouse model, we evaluated the therapeutic potential of epidermal growth factor (EGF) enema and epidermal growth factor receptor (EGFR) monoclonal antibody (mAb) injection as a treatment for IBD.
Materials and Methods
Twelve male C57BL/6 mice were divided into 4 groups (n=3 in each group), including a control group, model group, model group treated with EGF, and model group treated with EGF and EGFR mAb. Mice were sacrificed 9 weeks after disease symptoms first appeared. Colon tissues were then analyzed for histological changes, and protein expression levels of EGFR, Ki-67, p-AKT, and p-ERK were evaluated using immunohistochemistry and Western blotting.
Results
The AOM/DSS model exhibited significant weight loss and inflammation-driven colon damage compared to baseline at week 2; however, by the end of the study, body weight showed a trend toward recovery, with no significant differences observed between the groups. Histological analysis indicated partial improvement in the EGF group, and the combination treatment reduced inflammation compared to the model group. Both treatments significantly reduced Ki67 expression, with no significant difference between the EGF and combination treatments. Additionally, both treatments led to a decrease in p-Akt and p-ERK1/2
Conclusion
EGF enema and EGFR mAb injection exhibited significant therapeutic effects against AOM/DSS-induced IBD