Glial cell line-derived neurotrophic factor improves impaired colonic motility in experimental colitis mice through connexin 43

作     者：Wei Yang Rui Liu Feng Xu 

作者机构：Department of GastroenterologyThe First Affiliated Hospital of Zhengzhou UniversityZhengzhou 450052Henan ProvinceChina Medical SchoolXiangyang Vocational and Technical CollegeXiangyang 441021Hubei ProvinceChina 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志(英文))

年 卷 期：2025年第31卷第8期

页      面：82-95页

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

主　　题：Glial cell line-derived neurotrophic factor Ulcerative colitis Colonic motility Connexin 43 Dextran sodium sulfate model 

摘      要：BACKGROUND Colonic motility dysfunction is a common symptom of ulcerative colitis(UC),significantly affecting patients’quality of *** suggests that glial cell line-derived neurotrophic factor(GDNF)plays a role in restoring colonic *** To investigate whether GDNF enhances aberrant colonic motility in mice with experimental colitis via connexin 43(Cx43).METHODS An experimental colitis model was induced in male C57BL/6 mice using dextran sodium sulfate(DSS).The measurement of colonic transit time was conducted,and colon tissues were evaluated through transmission electron microscopy and hematoxylin and eosin *** mice were treated with exogenous GDNF and Gap 19,a selective Cx43 *** Cx43 and GDNF levels were detected via immunofluorescence,immunohistochemistry,and real-time polymerase chain *** levels of inflammatory markers,including interleukin-1β,tumor necrosis factor-α,interleukin-6,and C-reactive protein,were quantified using enzyme-linked immunosorbent *** Experimental colitis was successfully induced using DSS,and the findings exhibited that the colonic transit time was significantly delayed in colitis mice relative to the UC group(P0.01).GDNF treatment improved colonic transit time and alleviated intestinal inflammation in DSS-induced colitis mice(P0.05).In the UC+Gap19+GDNF group,colitis symptoms,colonic transit time,and inflammatory marker levels remained comparable to those in the UC group,indicating that the therapeutic effects of GDNF in UC mice were blocked by Gap *** GDNF improves colonic motility in mice with experimental colitis through a partially Cx43-mediated *** holds promise as a therapeutic option for improving colonic motility in patients with colitis.