Regulation of Colonic Motility by Cystathionine γ-Lyase Neuron Remodeling

Colitis is a colonic inflammatory reaction induced by various factors, such as pathogenic microorganisms, physical and chemical factors, and food allergens. At present, the mechanism of colonic motility disorder in colitis remains unclear. The aim of the present study was to investigate the relationship between the expression of cystathionine γ-lyase (CSE) in neurons from colonic tissue and colonic motility disorders in colitis.

A model of colitis was established in rats. The disease activity index (DAI) was determined in the colitis model and control rats, and the number of fecal droppings was recorded for 7 days. Organ bath recordings, immunohistochemistry, immunocytochemistry, and Western blotting were performed on rat colonic samples and in neurons of the myenteric plexus of the enteric nervous system (ENS) in order to investigate the relationship between the expression of CSE and colonic motility disorder in colitis.

In the colitis model, colonic motility and the number of fecal pellets were reduced. In addition, treatment with acetylcholine increased the contractile activity of colonic strips in both groups. Treatment with inhibitors of hydrogen sulfide (H₂S)-producing enzymes significantly increased the area under the curve of longitudinal muscle strips in the colitis group. CSE was expressed in the mucosa, submucosa, circular muscle, longitudinal muscle cells, and myenteric plexus. The expression of CSE in neurons of the myenteric plexus of the ENS was upregulated in the colitis group.

These findings suggest that upregulation of endogenous H₂S synthetase and increased H₂S production may account for decreased colonic motility.