Published online Aug 7, 2022. doi: 10.3748/wjg.v28.i29.3854
Peer-review started: December 16, 2021
First decision: April 16, 2022
Revised: April 27, 2022
Accepted: July 6, 2022
Article in press: July 6, 2022
Published online: August 7, 2022
Processing time: 229 Days and 18.6 Hours
Ulcerative colitis (UC) is a nonspecific inflammatory intestinal disorder with a complex etiology and poorly understood pathogenesis. The association between abnormal intestinal motility and UC has gained increasing attention over the past years. The enteric nervous system (ENS) regulates gut motility and based on their functions, has been divided into inhibitory and excitatory neurons, which mainly regulate the gut motility in terms of relaxation and contraction via different neurotransmitters. Nitrergic neurons are typical inhibitory neurons in the ENS and act through the neurotransmitter nitric oxide, which is synthetized by the rate-limiting enzyme nitric oxide synthase (NOS), whose expression changes might affect the motor function of the gut.
UC is an intestinal disease with abdominal pain and diarrhea as the main symptoms, which are associated with abnormal gastrointestinal motility. Alterations in the amount of enteric neurotransmitters may change the number of enteric neurons. Nitrergic neurons are well-established enteric inhibitory neurons, and modification of its expression may interfere with its regulatory effect on intestinal motility and improve the symptoms of abdominal pain and diarrhea in UC.
This study aimed to investigate the relationship between colonic NOS expression changes and colonic motility in dextran sulfate sodium (DSS)-induced UC rats, and to explore the effects of nitrergic neurons on colonic motility in UC rats to discover the potential mechanisms for the treatment of UC.
UC was induced in adult male rats with 5.5% DSS, and part of them were administered with NOS agonists and inhibitors. The rats were divided into control (CG), UC (EG1), UC + agonist (EG2), and UC + inhibitor (EG3) groups. The changes in tissue expression, relative protein expression, and concentration of NOS in rats were detected by immunofluorescence histochemical double staining, Western blot, and ELISA techniques, respectively. The effect of nitrergic neurons on colonic motility was examined by the changes in colonic circular muscle (CM) and longitudinal muscle (LM) contraction tension in vitro.
Compared with CG rats, the proportion of NOS positive neurons within the colonic myenteric plexus (MP), the relative expression of NOS, and the concentration of NOS in both serum and colonic tissue were significantly higher in EG rats. After administration of NOS agonists and inhibitors, various degrees of increase and decrease were observed in EG2 and EG3 rats, respectively. The contraction amplitude and mean contraction tension of the CM and LM in rat colon after administration of agonists and inhibitors were attenuated and enhanced in vitro, respectively. For UC, regulating the expression of NOS within the MP may improve intestinal motility, thereby favoring the recovery of intestinal function.
Nitrergic neurons within the rat colonic MP are involved in the regulation of colonic motility. Increased NOS in the colonic MP of UC rats causes nitrergic neurons amplification, leading to decreased colonic contraction function. Modulation of NOS levels within colonic MP can alter nitrergic neuron expression and adjust the motor activity of the intestinal smooth muscle, which can further improve colonic motor function, moderate UC symptoms, and provide evidence for the development of new drugs against UC.
This study demonstrated increased NOS expression in the colonic MP of UC rats, with a possible corresponding increase in nitrergic neuron expression and a decrease in colonic contraction function in UC rats. Thus, by regulating the expression of NOS in the colonic MP, colonic motor function and interruption in the pathogenesis of UC can be achieved, thus providing a novel insight into the treatment of UC.