Glial-Derived Neurotrophic Factor Improves Impaired Colonic Motility in Mice of Ulcerative Colitis through Connexin 43

(1) Background: Impaired colonic motility is common in patients with ulcerative colitis. The patients often complain the symptoms related to colonic motility dysfunction such as loose stools or diarrhea and these symptoms make therapy more challenging; (2) Methods: This study aimed to examine the movement of the colon in mice with ulcerative colitis and determine if the glial-derived neurotrophic factor (GDNF) may enhance aberrant colonic motility through Connexin 43 (Cx43).A model of ulcerative colitis was created using 32 male C57BL/6 mice. Colonic transit time was measured in all mice, and colon tissues were examined using hematoxylin-eosin staining (HE) and transmission electron microscopy (TEM). The levels of GDNF and Cx43 were determined via immunohistochemistry, immunofluorescence, and RT-PCR techniques. The levels of C-reactive protein (CRP),TNF-α, IL-1β, and IL-6 were quantified using the enzyme-linked immunosorbent assay (ELISA); (3) Results: 1) The UC models were effectively established by administering dextran sodium sulfate (DSS) water. Mice with ulcerative colitis exhibited a delay in colonic transit time. 2) GDNF can improve the delayed movement of the colon in mice with UC by activating the Cx43 protein; (4) Conclusions: GDNF can ameliorate impaired colonic motility in mice with ulcerative colitis, and its mechanism is related to the activity of Cx43. GDNF could potentially be utilized as a therapeutic option for addressing aberrant colonic motility in patients.