Abstract
Background Rifaximin is effective in relieving pain symptoms with IBS patients, although the mechanisms were not clear. The aims of the research were to investigate whether the visceral hyperalgesia was alleviated by rifaximin via TRPV1 channel in rats. Methods Rats were subjected to water avoidance stress (WAS) and were pretreated with rifaximin by oral gavage. The visceromotor response to colorectal distension was measured. The changes of TRPV1 in peripheral and central neurons of rats were detected by immunofluorescence, western blot method, and RT-PCR. Bacterial 16S ribosomal DNA in ileal contents was assessed using the Illumina MiSeq platform. The effect of intestinal flora on TRPV1 channel was observed by fecal microbiota transplantation (FMT) methods. Results Rifaximin could relieve the visceral hyperalgesia and reduce the TRPV1 expression of neurons and ileum mucosa in rats induced by WAS. The reduced relative abundance of intestinal flora induced by WAS could be partly prevented by rifaximin. The electromyographical activities and immunoreactivity of TRPV1 in rats could be changed after FMT. Conclusions Rifaximin could improve visceral hyperalgesia via TRPV1 channels of peripheral and central neurons by modulating intestinal flora in rats.
Highlights
Irritable bowel syndrome (IBS) is the most common functional gastrointestinal disorder that affects approximately 10-20% of the world’s population [1]
Intestinal flora was involved the development of visceral hyperalgesia in rats, our research indicated that antibiotic rifaximin reduced the pain threshold in water avoidance stressed rats, which were associated with the imbalance of Shannon index Control
Further researches showed that fecal microbiota transplantation (FMT) induced the change of transient receptor potential vanilloid 1 (TRPV1) signal protein from peripheral and central neurons, and that results in visceral hyperalgesia
Summary
Irritable bowel syndrome (IBS) is the most common functional gastrointestinal disorder that affects approximately 10-20% of the world’s population [1]. Studies indicated that visceral hyperalgesia, increased sensation pressure threshold to rectal distention, was one of the important pathogenesis of abdominal pain in patients with IBS [2]. The brain signals from visceral afferents may be affected by various stimuli which interacted with the intestinal flora. Rifaximin is effective in relieving pain symptoms with IBS patients, the mechanisms were not clear. The aims of the research were to investigate whether the visceral hyperalgesia was alleviated by rifaximin via TRPV1 channel in rats. The effect of intestinal flora on TRPV1 channel was observed by fecal microbiota transplantation (FMT) methods. Rifaximin could relieve the visceral hyperalgesia and reduce the TRPV1 expression of neurons and ileum mucosa in rats induced by WAS. Rifaximin could improve visceral hyperalgesia via TRPV1 channels of peripheral and central neurons by modulating intestinal flora in rats
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