Abstract
Postinflammatory irritable bowel syndrome (PI-IBS) is a common functional gastrointestinal disorder, which is characterized by abdominal pain, low-grade inflammation, and visceral hypersensitivity. Shaoyao-Gancao decoction (SGD) has been used to improve the clinical symptoms of abdominal spasmodic pain accompanying acute gastroenteritis, but the underlying therapeutic mechanism has not been fully elucidated. In the present study, a rat model of PI-IBS was established via rectal administration of TNBS. Rats were scored daily for 28 days using disease activity index (DAI). Abdominal withdrawal reflex (AWR) was used to measure the pain threshold. After SGD (6.25, 12.5, and 25 g/kg/d) treatment for 14 days, rat colonic tissue was collected for histopathological grading, enterochromaffin (EC) cell count, and 5-HT content measurement. RT-qPCR and western blot analyses were employed to detect the gene and protein level of tryptophan hydroxylase (TPH), serotonin reuptake transporter (SERT), and transient receptor potential vanilloid 1 (TRPV1). To further validate the effect of SGD on TRPV1, another experiment was performed in cells. The results revealed that visceral hyperalgesia, reflected by increased DAI, AWR, pathological injury score, 5-HT content, and EC cell count in PI-IBS rats, was significantly ameliorated by SGD. In cells, SGD markedly inhibited the expression and function of TRPV1. Moreover, the expression levels of TPH were also repressed by SGD. The findings of the present study indicated that the therapeutic effect of SGD on visceral hyperalgesia may be closely associated with the regulatory role of TRPV1 and 5-HT signaling pathways.
Highlights
As one of the most common functional gastrointestinal disorders, irritable bowel syndrome (IBS) is characterized by abdominal pain and altered bowel habits, with a prevalence of 10–20% in the general population [1]
Following treatment with Shaoyao-Gancao decoction (SGD), the Abdominal withdrawal reflex (AWR) increased in a dose-dependent manner. e result indicated that SGD exerted an analgesic effect on postinflammatory IBS (PI-IBS) rats
The transient receptor potential vanilloid 1 (TRPV1) expression level was found to be significantly increased in nerve fibers of IBS patients [30]. Consistent with these results, the present study demonstrated that the gene and protein levels of TRPV1 were significantly increased in PI-IBS rats and that SGD treatment could reverse this increase
Summary
As one of the most common functional gastrointestinal disorders, irritable bowel syndrome (IBS) is characterized by abdominal pain and altered bowel habits, with a prevalence of 10–20% in the general population [1]. Multiple triggering events are involved in IBS pathophysiology, including psychosocial disturbance, low-grade inflammation, visceral hypersensitivity, and altered microbiota, but the precise mechanisms remain elusive [2]. Patients with PI-IBS have more evident visceral hypersensitivity compared with IBS [3, 4], which may severely disrupt their daily life. Visceral hypersensitivity is considered as the common clinical feature among all PI-IBS patients [5]. The underlying mechanisms remain unclear, multiple evidence indicates that a variety of neuron-localized ion channels, such as transient receptor potential (TRP), serotonin (5HT), and gut mucosal mast cells and their mediator, histamine, play key roles in the process of PI-IBS [6].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Evidence-Based Complementary and Alternative Medicine
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
