Research on the mechanism of 25-hydroxycholesterol in inflammatory bowel disease in mice
10.19405/j.cnki.issn1000-1492.2025.07.006
- Author:
Yutong Li
1
;
Xiaoqi Luo
1
;
Qifa Tan
2
;
Mingjie Chen
1
;
Changyou Wu
3
;
Juan Shen
1
Author Information
1. KingMed School of Laboratory Medicine，Guangzhou Medical University，Guangzhou 511436; Guangzhou Key Laboratory for Clinical Rapid Diagnosis and Early Warning of Infectious Diseases， Guangzhou 511436; Engineering Technology Research Center of Intelligent Diagnosis for Infectious Diseases in Guangdong Province，Guangzhou 511436
2. Dept of Laboratory Medicine，The Third People 's Hospital of Ganzhou City，Ganzhou 341000
3. Institute of Immunology，Zhongshan School of Medicine， Sun Yat-sen University，Guangzhou 511400
- Publication Type:Journal Article
- Keywords:
interleukin-17;
25-hydroxycholesterol;
inflammatory bowel disease;
RORγt;
γδT cells;
mucosal damage
- From:
Acta Universitatis Medicinalis Anhui
2025;60(7):1204-1212
- CountryChina
- Language:Chinese
-
Abstract:
Objective :To explore the role and mechanism of 25-hydroxycholesterol (25-HC) in inflammatory bow- el disease (IBD) in mice．
Methods :All mice were divided into three groups : the control group was fed normally ; the DSS model group was fed with 2. 5% dextran sulfate sodium (DSS) solution ; the DSS + 25-HC experimental group was fed with 2. 5% DSS solution and he mice in the experimental group were intraperitoneally injected with 25-HC．The symptom changes of the mice were evaluated by assessing the disease activity index(DAI) ，and the tis- sue changes were judged by histological scoring．The expression of interleukin-17 and its signaling pathways in the mice were detected by Western blot，qRT-PCR, immunohistochemistry /fluorescence，and flow cytometry．Combined with the detection of tight junction proteins in the intestinal epithelium of the mice，the mechanism by which 25-HC affects IBD in mice was explored．
Results :In comparison to the DSS control group，The DSS + 25-HC experimen- tal group mice exhibited a reduction in body weight ( F = 30. 1，P ＜0. 000 1) ，a shortened colon ( F = 63. 8，P < 0. 05) ，and elevated DAI(F = 774. 5，P＜0. 000 1) and histopathological scores(F = 141. 5，P＜0. 05) ．Addition- ally，the expression of tight junction-associated proteins(ZO-2，Occludin，JAM and Claudin-4) was found to be sig- nificantly reduced．The level of IL-17 significantly decreased，and its expression level was positively correlated with tight junction proteins．
Conclusion :25-HC inhibited IL-17 production by colonic γδ T cells through the RORγt pathway，aggravated mucosal injury，and promoted the development of DSS-induced acute colitis in mice．
- Full text:202603041725562584425-羟基胆固醇参与小鼠炎症性肠病的机制_李雨桐.pdf
