Chronic Superficial Gastritis Patients Research Articles

Metabolomic profiling of plasma reveals potential biomarkers for screening and early diagnosis of gastric cancer and precancerous stages

AbstractGastric cancer (GC) faces a great challenge in clinical diagnosis, that it often is detected at advanced stages and there is a loss of optimum time for treatment. Thus, it is necessary to develop effective strategies for diagnosis of GC. In this study, 82 participants were enrolled, including 50 chronic superficial gastritis (CSG) patients, 7 early gastric cancer (EGC), and 25 advanced gastric cancer (AGC) ones. Metabolites profiling on patient plasma was performed. Furthermore, the proposed biomarkers were used to create random forest models, in which discrimination efficiency and accuracy were ascertained by receiver operating characteristic (ROC) curve analysis. l‐carnitine, l‐proline, pyruvaldehyde, phosphatidylcholines (PC) (14:0/18:0), lysophosphatidylcholine (14:0) (LysoPC 14:0), lysinoalanine were defined as the potential biomarker panel for the diagnosis among CSG and EGC patients. Compared with EGC patients, PC(O‐18:0/0:0) and LysoPC(20:4(5Z,8Z,11Z,14Z)) were found to be upregulated in AGC patients, whereasl‐proline, l‐valine, adrenic acid, and pyruvaldehyde downregulated. Pathway analysis revealed several metabolism disorders, involving amino acids and lipid metabolism. ROC analysis demonstrated a high diagnostic performance in disease diagnosis between CSG and GC. The above results indicate that the biomarker panels are sensitive to early diagnosis of GC disease, which is expected to be a promising diagnostic tool for disease stratification studies.

Differences in gastric microbiota and mucosal function between patients with chronic superficial gastritis and intestinal metaplasia.

Chronic superficial gastritis (CSG) and intestinal metaplasia (IM) can further develop into gastric cancer, which seriously endangers the health of people all over the world. In this study, the differences in gastric microbiota between CSG patients and IM patients were detected by 16S rRNA gene sequencing. As the expression levels of mucin and CDX2 are closely related to IM, the expression differences of mucin (MUC2 and MUC5AC) and CDX2 in the gastric mucosa of CSG patients and IM patients were detected by Western blot and qRT-PCR. The results showed that both Faith_pd and Observed_species indexes of microbiota in the gastric juice of CSG patients were significantly higher than those of IM patients. At the genus level, Thermus and Anoxybacillus were dominant in the gastric juice of IM patients, and Helicobacter was dominant in the gastric juice of CSG patients. Non-metric multidimensional scaling (NMDS) demonstrated that the dispersion of samples in the CSG group is greater than that in the IM group, and some samples in the CSG group are clustered with samples in the IM group. The KEGG metabolic pathway difference analysis of gastric juice microbiota in CSG and IM patients revealed that the gastric juice microbiota in the CSG and IM patients were significantly enriched in the amino acid metabolism, carbohydrate metabolism, and metabolism of cofactors and vitamins, and the functional differences between the two groups were mainly concentrated in the bacterial secretion system (VirB1, VirB2, VirB3, VirD2, and VirD4). In conclusion, there are significant differences in gastric microbiota and mucosal function between the CSG and IM patients. Moreover, the results of this study may provide a new means for the detection of CSG and IM and a new direction for the prevention and treatment of CSG and IM.

Effect of gastric microbiota on quadruple Helicobacter pylori eradication therapy containing bismuth.

BACKGROUND Helicobacter pylori (H. pylori) is an important pathogen that can cause a variety of diseases. Yet, full eradication of H. pylori remains a significant challenge in clinical practice. H. pylori and other microbial communities have complex interactions in the unique gastric microecological environment. However, it is not clear whether the interactions have any effect on the therapeutic effect of H. pylori.AIMThe aim was to investigate the characteristics of the gastric microbiota with H. pylori infection and the influence on the H. pylori eradication treatment.METHODSPatients with H. pylori infection underwent gastroscopy and received treatment for eradication. The prescription included esomeprazole 20 mg bid, Livzon Dele 220 mg bid, amoxicillin 1000 mg bid, and clarithromycin 500 mg bid for 14 d. Patients who did not respond to treatment and failed eradication were compared with those who achieved eradication by 1:2 propensity matching. High-throughput sequencing of the gastric mucosal microbiota was performed, and the results were evaluated by alpha diversity analysis, beta diversity analysis, species correlation analysis, and metabolic pathway correlation analysis.RESULTSThe eradication rate of all the patients was 95.5% (171/179). Twenty-four patients were enrolled in the study after propensity-matched scoring. There were eight cases in the failure group (patients who did not respond well to therapy) and 16 cases in the success group. The majority phyla in the two groups were the same, and included Proteobacteria, Bacteroides, Firmicutes, Actinomycetes, and Fusobacteria. The microbial diversity in the failure group had a decreasing trend (P = 0.092) and the species abundance was significantly lower (P = 0.031) compared with the success group. The high rate of H. pylori eradication was associated with Rhodococcus, Lactobacillus, and Sphingomonas, as they were significantly enriched in the successful group (P < 0.05). Veronococcus and Cilium were enriched in the mucosa of chronic atrophic gastritis patients compared with chronic superficial gastritis patients (P = 0.0466 and 0.0122, respectively). In both study groups, H. pylori was negatively correlated with other bacterial genera. More bacterial genera were directly related to H. pylori in the successful group compared with the failure group.CONCLUSIONThe effectiveness of quadruple H. pylori eradication therapy containing bismuth depended on gastric microbiota, and the high rate of H. pylori eradication was associated with the presence of Rhodococcus, Lactobacillus, and Sphingomonas.

The Mechanisms of Sijunzi Decoction in the Treatment of Chronic Gastritis Revealed by Network Pharmacology.

Chronic gastritis is characterized by inflammation in the gastric mucosa with a vicious circle in inflammatory cells and inflammatory mediators. Stomach adenocarcinoma would occur in the metaplastic gastric mucosa of chronic gastritis. Sijunzi decoction is a famous classical formula for the treatment of chronic gastritis. Although previous studies revealed some functions of Sijunzi decoction in treating chronic gastritis, the underlying mechanisms have not been illustrated clearly. In this study, we used network pharmacology to investigate the mechanism of Sijunzi decoction in treating chronic gastritis. Firstly, online datasets TCMSP, SWISS, and DisGeNET were used to investigate the functional mechanism of Sijunzi decoction against chronic gastritis and 18 genes were identified as targets of Sijunzi decoction in chronic gastritis. These 18 genes can be categorized into immunologically related genes and cancer-related genes. GO analysis showed that the 18 target genes were mainly enriched in angiogenesis, nitric oxide biosynthetic process, ERK1 and ERK2 cascade, cellular response to drug, and MAPK cascade. So, Sijunzi decoction alleviated chronic gastritis by inhibiting the local inflammatory response. Furthermore, we also investigated the impact of Sijunzi decoction on the peripheral blood leukocytes with our own RNA sequencing (RNA-seq) data of 11 chronic superficial gastritis patients. 102 differentially expressed genes (DEGs) were identified by comparing RNA-seq data of chronic superficial gastritis patients with healthy control groups. After performing a functional analysis on 102 DEGs and Sijunzi decoction potential targets and taking the intersection of these pathways, we found that platelet activation, angiogenesis, and pathways in cancer were candidate target pathways regulated by Sijunzi decoction. Thus, Sijunzi decoction also alleviates chronic gastritis by suppressing inflammatory response of peripheral blood leukocytes. Our results showed that Sijunzi decoction can ameliorate the local gastric inflammation and inflammations in peripheral blood leukocytes and might also reduce the incidence of stomach cancer in chronic gastritis.

Screening for blood leukocyte microRNA biomarkers responsible for association between qi deficiency constitution and Pi-qi-deficiency syndrome of chronic superficial gastritis

Abstract Objective To screen for blood leukocyte microRNA (miRNA) biomarkers responsible for the association between the traditional Chinese medicine (TCM) qi deficiency constitution (QDC) and the Pi-qi-deficiency syndrome (PQDS) of chronic superficial gastritis (CSG). Methods Peripheral blood leukocytes were separated from people of two TCM constitutions (balance and qi deficiency) and from CSG patients with PQDS. Total RNA was isolated from the leukocytes and subjected to subsequent high-throughput miRNA sequencing to identify the miRNAs that are specifically and highly expressed in persons of QDC and CSG patients with PQDS. In addition, the target genes of the associated miRNAs were predicted. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway-based enrichment analyses of these target genes were performed to further evaluate the associated miRNA candidates as potential biomarkers responsible for the association between QDC and PQDS of CSG. Results Compared with the control group with a balance constitution (P 1.5 or Conclusion Hsa-miR-145-5p and hsa-miR-146a-3p may serve as candidate biomarkers responsible for the association between QDC and PQDS of CSG.

Clinical Study on traditional Chinese medicine treatment of CSG and its impact on MTL, GAS and SS

Objective To discuss of the therapeutic effects of treating three TCM types of Chronic superficial gastritis （CSG）disharmony of liver and stomach, weakness of the spleen and the stomach, and damp heat in the spleen and the stomach with chinese medicine, and to discuss its impact on the changes of three gastrointestinal hormones-- motilin （MTL）, gastrin （GAS）, and somatostatin （SS）. Methods The data of 150 CSG patients in Shenzhen Bao’an Hospital from Feb, 2011 to Mar, 2013 were selected. These patients belonged to three kinds of syndrome, which was disharmony of liver and stomach, weakness of the spleen and the stomach, and damp heat in the spleen and the stomach, each syndrome had 50 cases. Different Chinese medicines were applied to different syndrome of patients. After one month treatment, the therapeutic effects and the changes of MTL, GAS, SS in these patients were detected by radioimmunoassay. Results After treatment, the total effective rate of the damp heat in the spleen and the stomach syndrome was 94%, the weakness of the spleen and the stomach type was 88%, disharmony of liver and stomach type was 90%, the difference was not statistically significant among the three types（χ2=3.84, P〉0.05）;after treatment, the serum MTL, SS level of disharmony of liver and stomach, weakness of the spleen and the stomach, and damp heat in the spleen and the stomach type were [damp heat in the spleen and the stomach type were （240.25±7.29）pg/ml, （68.23± 5.97）pg/ml;the weakness of the spleen and the stomach type were （260.16±8.84）pg/ml, （75.35±4.65）pg/ml;disharmony of liver and stomach type were（258.32±15.23）pg/ml, （80.12±7.88）pg/ml] higher than before treatment [damp heat in the spleen and the stomach type were （87.26±7.58）pg/ml, （49.34±4.93）pg/ml;the weakness of the spleen and the stomach type were （67.11±7.81）pg/ml, （57.15±5.11）pg/ml; disharmony of liver and stomach type were （89.26±7.60）pg/ml, （40.63±7.26）pg/ml], and the levels of serum GAS＆amp;nbsp;[（156.38±17.36）pg/ml, （146.15±15.56）pg/ml, （140.26±13.37）pg/ml] was lower than before treatment [（274.59 ± 17.82）pg/ml, （320.83 ± 15.02）pg/ml, （216.15 ± 13.77）pg/ml], the difference was statistically significant （P〈0.05 or 0.01）. Conclusions The changes of three hormones-MTL, GAS, SS can be used as an objective basis for the diagnosis and the judgment of healing efficacy of CSG treated by traditional Chinese medicine. Key words: Chronic superficial gastritis; Motilin; Gastrin; Somatostatin; Traditional chinese medicine treatment

Far Upstream Element-Binding Protein 1 (FUBP1) is Overexpressed in Human Gastric Cancer Tissue Compared to Non-Cancerous Tissue

Background: The aim of this study was to investigate the role of far upstream element-binding protein 1 (FUBP1) in gastric cancer development. Patients and Methods: Using immunohistochemistry, we detected FUBP1 expression in 18 chronic superficial gastritis patients, 33 chronic atrophic gastritis patients, 21 moderate and severe gastric dysplasia patients, and 31 gastric cancer patients. FUBP1 mRNA expression in gastric cancer tissue and paraneoplastic tissue was measured with fluorescent quantitative reverse transcription polymerase chain reaction. Results: The FUBP1 expression rates in the chronic atrophic gastritis, moderate and severe dysplasia, and gastric cancer patients were 51.51% (17/33), 76.19% (16/21), and 90.32% (28/31), respectively; these were higher than the expression rate of the chronic superficial gastritis patients (11.11%, 2/18). FUBP1 expression in the gastric cancer patients was significantly higher than that in the chronic atrophic gastritis patients. The relative amount (0.2593 ± 0.1209) of FUBP1 mRNA in the gastric cancer tissue was higher than that in paraneoplastic tissue (0.1969 ± 0.0211) (p < 0.05). There was a statistically significant correlation between overall survival rates and age, sex, lymph node metastasis, and distant metastasis (p < 0.05). Conclusion: FUBP1 expression differs among gastric tissues. There is a correlation between overall survival rates and age, sex, lymph node metastasis, and distant metastasis.

Cancer Stem Cells Biomarkers in Gastric Carcinogenesis

Gastric carcinogenesis is a multistep process, involving multiple molecular alterations, including changes in cancer stem cells (CSCs). The present investigation was undertaken to determine whether changes in cancer stem cells could be utilized as a marker of progression of gastric carcinogenesis by examining the expression of gastric CSCs at different stages of carcinogenesis. Ninety-three cases with 31 in each group of chronic superficial gastritis (CSG), chronic atrophic gastritis (CAG), or gastric cancer (GC) were analyzed immunohistochemically for proliferating cell nuclear antigen (PCNA) and Bcl-xl as biomarkers of proliferation and apoptosis, respectively, and CD44, CD166, and LGR5 levels by qRT-PCR as markers of gastric CSCs. Additionally, the levels of P53 and phosphorylated form of epidermal growth factor receptor (p-EGFR) were examined. While the levels of each of these biomarkers were found to be low to moderate in CSG and CAG patients, they were markedly increased in GC patients, in whom co-expression of CD44 with LGR5 and CD166 with p-EGFR was found to be the highest. We have also observed that although the expression of different CSC markers as well as the levels of p-EGFR were increased in precancerous lesions (CSG and CAG), they are further augmented in GC suggesting that they may play a pivotal role in the development and progression of gastric cancer. Our observations suggest that the progression to gastric carcinogenesis from preneoplastic lesions such as superficial gastritis and chronic atrophic gastritis is associated with induction of CSCs together with increase in cell proliferation and inhibition of apoptosis.

Increased expression of matrix metalloproteinase-9 associated with gastric ulcer recurrence

To compare matrix metalloproteinase (MMP)-9 and tissue inhibitor of metalloproteinase (TIMP)-1 in gastric ulcer (GU) and chronic superficial gastritis (CSG). This study enrolled 63 patients with GU and 25 patients with CSG. During upper gastroduodenal endoscopy, we took samples of gastric mucosa from the antrum and ulcer site from patients with GU, and samples of antral mucosa from patients with CSG. Mucosal biopsy tissues were cultured for 24 h, and the culture supernatant was measured for levels of MMP-9 and TIMP-1. After receiving eradication therapy for Helicobacter pylori (H. pylori) and 8 wk proton-pump inhibitor therapy for GU, follow-up endoscopy examination was performed after 6 mo and whenever severe symptoms occurred. Levels of MMP-9 and TIMP-1 at the ulcer site or in the antrum were significantly higher in GU than CSG patients. MMP-9 levels at the ulcer site were significantly higher than in the antrum in GU patients, and had a significantly positive correlation with TIMP-1. MMP-9 levels were significantly higher in H. pylori-positive than H. pylori-negative GU and CSG patients. Levels of MMP-9 or TIMP-1 at the ulcer site were associated with the histological severity of activity and inflammation. About 57 GU patients were followed up, and seven had GU recurrence. H. pyloriinfection and MMP-9 levels were risk factors for the recurrence of GU adjusted for age and sex by multiple logistic regression analysis. MMP-9 may perform an important function in gastric ulcer formation and recurrence.

Correlations among Helicobacter pylori infection and the expression of cyclooxygenase‐2 and vascular endothelial growth factor in gastric mucosa with intestinal metaplasia or dysplasia

To examine the rate of Helicobacter pylori infection and the expression of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) in gastric mucosa with intestinal metaplasia or dysplasia, and explore their correlations in precancerous gastric lesions. A total of 172 patients were included in the study. H. pylori infection was evaluated by hematoxylin-eosin and modified Giemsa staining. The expression of COX-2 and VEGF proteins was detected by immunohistochemistry. The rates of H. pylori infection in gastric mucosal dysplasia (DYS), intestinal metaplasia in gastric mucosa (IM), chronic atrophic gastritis (CAG) and chronic superficial gastritis (CSG) patients were significant differences (P = 0.001). The average optical density (AOD) values of COX-2 staining in CSG, CAG, IM and DYS patients were 13.81 +/- 5.53, 45.28 +/- 21.44, 73.67 +/- 26.02 and 91.23 +/- 45.11, respectively, with significant differences among CSG, CAG and IM patients (P = 0.037, 0.001 and 0.047 for CSG vs CAG, CSG vs IM and CAG vs IM, respectively). The expression level of VEGF in DYS patients was significantly higher than those in other patients (P = 0.001, 0.001 and 0.001 for DYS vs CSG, DYS vs CAG and DYS vs IM, respectively). The expression levels of COX-2 in H. pylori-positive IM, CAG and DYS patients were significantly higher than those in H. pylori-negative counterparts (P = 0.043, 0.009, 0.001, respectively). Additionally, the expression level of COX-2 was positively correlated with that of VEGF with the aggravation of gastric mucosal lesions (r = 0.640, P = 0.006). H. pylori infection might be able to induce the expression of COX-2 in precancerous gastric lesions, which in turn upregulates the expression of VEGF.

Relationship between gene expressions of aquaporin 3 and 4 and various degrees of spleen-stomach dampness-heat syndrome in chronic superficial gastritis

To explore the relationship between gene expressions of aquaporin (AQP) 3 and 4 and various degrees of spleen-stomach dampness-heat syndrome in chronic superficial gastritis (CSG). Twenty-four CSG patients were divided into three groups according to the degrees of spleen-stomach dampness-heat syndrome: mild, moderate and severe groups. There were 8 patients in each group, and another 8 healthy persons were selected as normal control. Samples of mucosa of upper stomach in the included patients and normal persons were collected by gastroscopy, and then were stored in liquid nitrogen. The gene expressions of AQP3 and AQP4 in gastric tissue were examined by fluorescence quantitative polymerase chain reaction. The gene expressions of AQP3 and AQP4 in the moderate and severe groups were higher than that in the mild group and normal group (P<0.05, P<0.01). The gene expression of AQP3 in the severe group was higher than that in the moderate group (P<0.05). The gene expressions of AQP3 and AQP4 in gastric mucosa are different in patients with various degrees of spleen-stomach dampness-heat syndrome of CSG. There is a relationship between expressions of AQP3 and AQP4 genes and the degrees of spleen-stomach dampness-heat syndrome, and the gene expressions will increase with the aggravation of the dampness-heat syndrome.

Bioinformatics research on chronic superficial gastritis of Pi-deficiency syndrome by gene arrays

To determine the bioinformatical characteristics of differential gene expression in patients with chronic superficial gastritis (CSG) with the Pi-deficiency syndrome (PDS) and those of the non-Pi-deficiency syndrome (non-PDS), i.e. patients of CSG with Pi-Wei dampnese-heat syndrome and healthy persons. With the BRB-Array Tools software package, original data collection and bioinformatic: analysis of gene arrays were conducted in 6 CSG patients of PDS (CSG-PDS), 6 CSG patients of non-PDS (CSG-nPDS), and 6 healthy volunteers (Normal). Compared with non-PDS, the gene expressions: in PDS with regards to protein synthesis, energy metabolism, immune reaction and ionic transport tended to be down-regulated, while those concerning secretion, cytoskeleton and ubiquitinization were up-regulated dominantly. The two kinds of samples, CSG-PDS/Normal and CSG-PDS/CSG-nPDS, have their respective gene expression profiles with different characteristics. Gene expression profile has certain referential significance in syndrome classification.

Relationship between Helicobacter pylori infection and expression of connexin (Cx) 32 and Cx43 genes in gastric cancer and gastric precancerous lesions

To investigate the expression of connexin (Cx)32 and Cx43 genes in gastric cancer and precancerous lesion, and to investigate the relation between the changes of expression of Cx32 and Cx43 genes and Helicobacter pylori (Hp) infection. Gastroscopy and biopsy of gastric mucosa were conducted on 33 patients with chronic superficial gastritis (CSG), 88 with precancerous lesion, and 70 with gastric cancer. Hp was detected by rapid urease test, basic fuchsin staining, and 14C-urea breath test. The CagA gene of Hp was determined by PCR. SABC immunohistochemical method was used to detect the expression of Cx32 and Cx43 genes in gastric mucosa biopsy specimens. The positive expression rates of Cx32 and Cx43 genes were 15.7% and 32.9% respectively in the gastric cancer patients, 51.1% and 54.5% in the patients with precancerous lesion, and 100.0% and 93.9% in the CSG patients. The positive Cx32 and Cx43 expression rates of the gastric cancer and precancerous lesion patients were significantly lower than those of the CSG patients (all P < 0.05). The positive Cx32 expression rate of the gastric cancer patients with Hp infection was 16.7%, not significantly different from that of the gastric cancer patients without Hp infection (13.6%). The positive Cx43 expression rate of the gastric cancer patients with Hp infection was 25%, significantly lower than that of the gastric cancer patients without Hp infection (50%, P = 0.039). The positive Cx32 and Cx43 expression rates and expression intensity of the precancerous lesion patients with Hp infection were all significantly lower than those of the precancerous lesion patients without Hp infection (all P < 0.05). The positive Cx43 expression rate of the gastric cancer patients with CagA+ Hp infection was 17.9%, significantly lower than that of the CagA- Hp group (55.6%, P = 0.027), however, the positive Cx32 expression rate of the gastric cancer patients with CagA+ Hp infection was 12.8%, not significantly different from that of the gastric cancer patients with CagA- Hp infection (33.3%, P = 0.159). The positive Cx32 and Cx43 expression rates of the CSG patients with CagA+ Hp and CagA- Hp infection were all 100%, but the expression intensity of the CagA+ Hp group was significantly lower than that of the CagA- Hp group (P = 0.032). The positive Cx32 and Cx43 expression rates after Hp eradication of the precancerous lesion patients with Hp infection were 97.9% and 91.7% respectively, both significantly higher than those before eradication therapy (41.4% and 44.8% respectively, both P < 0.05). However, the positive Cx32 and Cx43 expression rates of the precancerous lesion patients with Hp infection without Hp eradication were still 40% and 50%, not significantly different from those before treatment. The expression levels of Cx32 and Cx43 in gastric cancer and precancerous lesion decrease. The change of expression of Cx43 was associated with Hp infection, especially CagA+ Hp infection. Hp eradication in patients with precancerous lesion up-regulates the expression of Cx32 and Cx43.

Expression of peroxisome proliferators-activated receptor-gamma and cyclooxygenase-2 in Helicobacter pylori infection-associated diseases and significance thereof

To investigate the expression of peroxisome proliferators-activated receptor-gamma (PPAR-gamma) and cyclooxygenase-2 (COX-2) in Helicobacter pylori (Hp)-associated gastric mucosal lesions and the relations among them. Two-step immunohistochemical staining was used to detect the expression of PPAR-gamma and COX-2 proteins in the gastric biopsy specimens from 209 patients with lesions of gastric mucosa, including 75 cases of chronic superficial gastritis (CSG), 24 cases of chronic atrophic gastritis (CAG), and 90 cases of intestinal metaplasia (MI) and dysplasia (DYS), and from 20 subjects with normal gastric mucosa negative in Hp as controls. In addition, 36 CSG patients were followed up for 10 years to observe the changes of expression of PPAR-gamma and COX-2. (1) The expression of COX-2 protein in the glandular cells of the CSG, CAG, and IM + DYS groups were 42.7%, 45.8%, and 61.1% respectively, all significantly higher than that of the control group (20%, P < 0.01 or 0.05). The expression of COX-2 protein in the inflammatory cells of the CSG, CAG, and IM + DYS groups were 32%, 29.2%, and 36.7% respectively, all significantly higher than that of the control group (0%, all P < 0.05). (2) In the CSG and IM + DYS groups the expression levels of COX-2 in both the inflammatory and glandular cells were both significantly higher in the Hp-positive patients than in the Hp-negative patients (P < 0.05 or 0.01). (3) The expression of PPAR-gamma protein in the glandular cells of the CSG, CAG, and IM + DYS groups were 18.7%, 29.2%, and 45.6% respectively, all significantly higher than that of the control group (0%, all P < 0.01); and the expression levels of PPAR-gamma protein in the inflammatory cells of the CSG, CAG, and IM + DYS groups were 22.5%, 20.8%, and 22.2% respectively, all significantly higher than that of the control group (0%, P < 0.05 or 0.01). (4) In the CSG and IM + DYS groups the expression levels of PPAR-gamma in the inflammatory cells of the Hp-positive patients were both significantly higher than those of the Hp-negative patients (both P < 0.01); and the. expression levels of PPAR-gamma in the glandular cells of the Hp-positive patients were both significantly higher than those of the Hp-negative patients (both P < 0.01). (5) The expression level of COX-2 in the inflammatory cells of the CSG patients with a persistent Hp infection after a period of ten years was 33.3%, significantly lower than that a decade before (38.9%, P < 0.05). However, the expression level of PPAR-gamma in the inflammatory cells of the patients with a persistent Hp infection after a period of ten years was 30.6%, not significantly different from that a decade before (33.3%, P > 0.05). (6) The expression levels of COX-2 and PPAR-gamma in the glandular cells of the CSG patients with a persistent Hp infection after a period of ten years were 55.6% and 30.6% respectively, both significantly higher than those a decade before (47.2% and 22.2%, both P < 0.01). (7) In all Hp-negative disease groups the expression level of COX-2 in the inflammatory cells was not significantly correlated with the expression level of PPAR-gamma in the inflammatory cells(r = 0.006 and 0.149, P > 0.05) In the Hp-negative disease groups, the expression level of COX-2 in the glandular cells was significantly positively correlated with the expression level of PPAR-gamma in the glandular cells in the IM + DYS group (r = 0.336, P < 0.05), however, not significantly correlated with the expression level of PPAR-gamma in the glandular cells in both CAG and CSG groups (r = 0.035 and 0.126, both P > 0.05). (8) In both the inflammatory cells and glandular cells the COX-2 expression was significantly positively correlated with the PAR-gamma expression in all disease groups with Hp positivity (r = 0.348 and 0.645, P < 0.05 or 0.01). (1) Hp infection induces the overexpression of COX-2 and PPAR-gamma in the inflammatory and glandular cells within gastric mucosa, thus participating in the pathogenesis of gastric cancer (2) The expression of COX-2 induces by Hp is related to acute inflammation caused by Hp infection. In the glandular cells, significant increase of COX-2 and PPAR-gamma expression implies that along with time the expression of COX-2 and PPAR-gamma may change in advance of the morphological changes of the gastric mucosa.