Published online Mar 14, 2024. doi: 10.3748/wjg.v30.i10.1431
Peer-review started: November 27, 2023
First decision: December 12, 2023
Revised: December 29, 2023
Accepted: February 6, 2024
Article in press: February 6, 2024
Published online: March 14, 2024
Processing time: 108 Days and 4.1 Hours
Patients with irritable bowel syndrome with diarrhea (IBS-D) experience a significant reduction in their quality of life. While the exact pathogenesis of IBS-D remains incompletely understood, research indicates that serotonin receptor 2B (5-HT2B receptor) plays a critical role in many chronic pain conditions. The role of 5-HT2B receptor in the altered gut sensation of IBS-D was not investigated.
This study is to identify the role of 5-HT2B receptor in the altered gut sensation via transient receptor potential vanilloid type 1 (TRPV1) channels in rat model and patients with diarrhea-predominant IBS.
This study aims to elucidate the role of the 5-HT2B receptor in both IBS-D patients and rat models induced by acetic acid and wrap restraint. The findings are anticipated to offer novel insights into potential avenues for IBS-D treatment.
Rectosigmoid biopsies were collected from IBS-D patients and healthy controls. The expression level of 5-HT2B receptor in colon tissue was measured and correlated with abdominal pain scores in IBS-D patients. The IBS-D rat model was induced by intracolonic instillation of acetic acid and wrap restraint. Alterations in visceral sensitivity, 5-HT2B receptor and TRPV1 expression were examined following 5-HT2B receptor antagonist administration. Changes in visceral sensitivity after the administration of the TRPV1 antagonist were recorded.
A higher expression of 5-HT2B receptor was observed in the colonic mucosa of patients with IBS-D compared to controls, correlating with abdominal pain scores. The IBS-D rats was successfully established through intracolonic instillation of acetic acid and wrap restraint. Administration of the exogenous 5-HT2B receptor agonist increased visceral hypersensitivity, which was subsequently alleviated by successive administration of TRPV1 antagonist. IBS-D rats receiving the 5-HT2B receptor antagonist displayed inhibition of visceral hyperalgesia. Additionally, the percentage of 5-HT2B receptor-immunoreactive (IR) cells surrounded by TRPV1-positive cells (5-HT2B receptor I+) and total 5-HT2B receptor IR cells (5-HT2B receptor IT) in IBS-D rats significantly decreased with the administration of 5-HT2B receptor antagonist.
The increased expression of 5-HT2B receptor contributing to visceral hyperalgesia through the induction of TRPV1 expression in IBS-D, providing important insights into the potential mechanisms underlying IBS-D-associated visceral hyperalgesia.
The analgesic effect of RS-127445 in IBS-D rats suggests its potential as a novel treatment for IBS-D.