Interaction of Cyclooxygenase‐2 with Helicobacter pylori Induces Gastric Chronic Nonresolving Inflammation and the Formation of Syndrome of Internal Block of Static Blood in Helicobacter pylori‐Related Gastric Diseases

Abstract

Cyclooxygenase-2 (COX-2) is an inducible enzyme stimulated by various inflammatory factors (IFs). Chronic gastritis is a classic model of “inflammation-cancer transformation” and Helicobacter pylori-related gastric diseases (HPGD) are specific ones of this model. Traditional Chinese Medicine (TCM) syndromes could play a predictive role in gastric histopathological evolution. To search for early warning evidence about “inflammation-cancer transformation,” this study is about to explore interaction of COX-2 with Helicobacter pylori (Hp) in HPGD with different TCM syndromes. All included subjects underwent endoscopy and biopsy. Hp infection was detected by rapid urease test and methylene blue staining. Histopathological characteristics and COX-2 expression in gastric mucosa (GM) were, respectively, observed by hematoxylin-eosin and Elivision™ plus. SPSS 18.0 and Stata 11.0 statistical software packages were used for statistical analysis. Results of immunohistochemical staining in this study showed COX-2 expression in Hp-positive patients was stronger than that in Hp-negative ones. Spearman’ analysis indicated that degrees of both Hp infection and COX-2 expression were positively correlated with those of gastric inflammation and inflammatory activity. Compared with the relative normal group, both severe dysplasia group and gastric carcinoma group had more severe Hp infection and COX-2 expression. Compared with the nonsyndrome, syndrome of internal block of static blood (IBSB) had higher scores in semiquantitative analysis of COX-2 protein expression among TCM groups. Moreover, multivariate logistics regression analysis suggested that patients with Hp infection could increase the risk of IBSB. These results indicated that COX-2 interacting with Hp could play an important role in transforming gastric chronic nonresolving inflammation into carcinoma in subjects with HPGD, as well as inducing the formation of IBSB. HPGD together with IBSB could be an early warning evidence for GM with histopathological evolution from benign to malignant.

<p>Progress in Research on Colorectal Cancer-Related Microorganisms and Metabolites</p>

“…123 At present, the mechanism of colorectal tumors caused by Helicobacter pylori infection is not clear, but hypergastrinemia and the expression of cyclooxygenase-2 (COX-2) are currently considered to be possible mechanisms of CRC caused by Helicobacter pylori infection. 124 In animal experiments in mice, it was found that overexpression of gastrin can cause intestinal metaplasia-atypical hyperplasia and eventually gastric cancer in 20 months. 125 Therefore, there is a hypothesis that H. pylori infection may indirectly lead to CRC through changes in gastrin levels: H. pylori infection causes atrophic changes in the gastric mucosa and high gastrin levels through the negative feedback mechanism of gastric antrum G cells, thereby promoting colonic mucosa growth.…”

The Single-Nucleotide Polymorphism of miR-27a rs895819 and the Expression of miR-27a in Helicobacter pylori-Related Diseases and the Correlation with the Traditional Chinese Medicine Syndrome

“…Our previous research found that there was a close connection between TCM syndrome and HPGD. e TCM syndromes are a macroscopic manifestation of the pathological changes in gastric mucosa, which can reflect the pathological process of the gastric mucosa to a certain extent and can play a warning role in the evolution of gastric cancer [20][21][22]. Our study detected the SNPs of miR-27a rs895819 and the miR-27a expression in different stages of HPGD to explore the microscopic differences of TCM syndromes and interpret the mechanism of pathological changes in gastric mucosa from multiple perspectives and thus can provide an early warning basis for the clinic.…”