Related Experiment Video
Updated: Mar 30, 2026

In vitro Functional Characterization of Mouse Colorectal Afferent Endings
Published on: January 21, 2015
Inducible Nitric Oxide Synthase in the Duodenal Mucosa Is Associated with Mast Cell Degranulation in Patients with
Hai-Peng Yuan1, Xiao-Pei Li1, Wen-Rong Yang1
1Department of Gastroenterology, Tai'an Central Hospital, Tai'an, China.
Aim:
Functional dyspepsia (FD) is a clinical syndrome with chronic gastroduodenal symptoms without noticeable organic or systemic diseases. According to the Rome III consensus, FD can be subdivided into PDS (postprandial distress syndrome) and EPS (epigastric pain syndrome). Neurotransmitters are involved in the development and pathology of FD. However, the expression profiles of neurotransmitters in FD patients are not clear. This study aimed to investigate the expression profile of neurotransmitters in the duodenal mucosa of FD patients.
Methods:
A total of 48 FD patients treated at our hospital were included in this study: 23 patients with PDS and 25 patients with EPS. Another 21 healthy volunteers served as normal controls. The duodenal mucosa was biopsied with gastroscopy and examined with immunohistochemical staining against serotonin, substance P, inducible nitric oxide synthase (iNOS), and vasoactive intestinal peptide (VIP). Mast cells were identified with toluidine blue staining.
Results:
The duodenal iNOS levels were significantly higher in PDS patients than the normal controls (P<0.05). The expression of serotonin, substance P, and VIP did not differ significantly among the groups. Mast cell counts and the percentage of mast cells with degranulation were significantly higher in PDS and EPS patients than normal controls (P<0.001) In addition, iNOS expression levels were positively correlated with percentage of degranulating mast cells (r=0.321, P=0.008).
Conclusions:
In conclusion, duodenal iNOS may be involved in the pathogenesis of PDS.
More Related Videos
08:32Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells
Published on: March 16, 2017
09:44Functional Assessment of Intestinal Motility and Gut Wall Inflammation in Rodents: Analyses in a Standardized Model of Intestinal Manipulation
Published on: September 11, 2012
Related Concept Videos
Nitric Oxide Signaling Pathway
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
Peptic Ulcer Disease I: Introduction
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors