Correlation of chronic atrophic gastritis with gastric-specific circulating biomarkers.

BACKGROUND AND STUDY AIMS: It has been suggested that the combined detection of multiple serum biomarkers can effectively screen out the high-risk population of chronic atrophic gastritis in the general population. Therefore, it is necessary to establish an effective predictive model of chronic atrophic gastritis. PATIENTS AND METHODS: Serum biopsies were assessed using five stomach-specific circulating biomarkers pepsinogen I (PGI), PGII, PGI/II ratio, anti- H. pylori antibody, and gastrin-17 (G-17) to identify high-risk individuals and evaluate the risk of developing chronic atrophic gastritis. RESULTS: In the cross-sectional analysis, PGII, the PG ratio, G17, anti- H. pylori IgG were positively associated with the presence of chronic atrophic gastritis, and combined prediction of the five biomarkers was more accurate than single-factor prediction ((0.692 vs 0.54(PG1), 0.604 (PGⅡ), 0.616(PGI/II ratio), 0.629(G-17)). CONCLUSION: The combination of PGI, PGII, the PGI/II ratio, G17, and anti-H. pylori antibodies for serological analysis are helpful to screen chronic atrophic gastritis high-risk subjects from the general population and recommend that these people carry out further endoscopy and biopsy.

Deep learning-assisted diagnosis of chronic atrophic gastritis in endoscopy.

Background: Chronic atrophic gastritis (CAG) is a precancerous condition. It is not easy to detect CAG in endoscopy. Improving the detection rate of CAG under endoscopy is essential to reduce or interrupt the occurrence of gastric cancer. This study aimed to construct a deep learning (DL) model for CAG recognition based on endoscopic images to improve the CAG detection rate during endoscopy. Methods: We collected 10,961 endoscopic images and 118 video clips from 4,050 patients. For model training and testing, we divided them into two groups based on the pathological results: CAG and chronic non-atrophic gastritis (CNAG). We compared the performance of four state-of-the-art (SOTA) DL networks for CAG recognition and selected one of them for further improvement. The improved network was called GAM-EfficientNet. Finally, we compared GAM-EfficientNet with three endoscopists and analyzed the decision basis of the network in the form of heatmaps. Results: After fine-tuning and transfer learning, the sensitivity, specificity, and accuracy of GAM-EfficientNet reached 93%, 94%, and 93.5% in the external test set and 96.23%, 89.23%, and 92.37% in the video test set, respectively, which were higher than those of the three endoscopists. Conclusions: The CAG recognition model based on deep learning has high sensitivity and accuracy, and its performance is higher than that of endoscopists.

Mitochondrial GRIM-19 loss in parietal cells promotes spasmolytic polypeptide-expressing metaplasia through NLR family pyrin domain-containing 3 (NLRP3)-mediated IL-33 activation via a reactive oxygen species (ROS) -NRF2- Heme oxygenase-1(HO-1)-NF-кB axis.

Spasmolytic polypeptide-expressing metaplasia (SPEM), as a pre-neoplastic precursor of intestinal metaplasia (IM), plays critical roles in the development of chronic atrophic gastritis (CAG) and gastric cancer (GC). However, the pathogenetic targets responsible for the SPEM pathogenesis remain poorly understood. Gene associated with retinoid-IFN-induced mortality 19 (GRIM-19), an essential subunit of the mitochondrial respiratory chain complex I, was progressively lost along with malignant transformation of human CAG, little is known about the potential link between GRIM-19 loss and CAG pathogenesis. Here, we show that lower GRIM-19 is associated with higher NF-кB RelA/p65 and NLR family pyrin domain-containing 3 (NLRP3) levels in CAG lesions. Functionally, GRIM-19 deficiency fails to drive direct differentiation of human GES-1 cells into IM or SPEM-like cell lineages in vitro, whereas parietal cells (PCs)-specific GRIM-19 knockout disturbs gastric glandular differentiation and promotes spontaneous gastritis and SPEM pathogenesis without intestinal characteristics in mice. Mechanistically, GRIM-19 loss causes chronic mucosal injury and aberrant NRF2 (Nuclear factor erythroid 2-related factor 2)- HO-1 (Heme oxygenase-1) activation via reactive oxygen species (ROS)-mediated oxidative stress, resulting in aberrant NF-кB activation by inducing p65 nuclear translocation via an IKK/IкB partner, while NRF2-HO-1 activation contributes to GRIM-19 loss-driven NF-кB activation via a positive feedback NRF2-HO-1 loop. Furthermore, GRIM-19 loss did not cause obvious PCs loss but triggers NLRP3 inflammasome activation in PCs via a ROS-NRF2-HO-1-NF-кB axis, leading to NLRP3-dependent IL-33 expression, a key mediator for SPEM formation. Moreover, intraperitoneal administration of NLRP3 inhibitor MCC950 drastically attenuates GRIM-19 loss-driven gastritis and SPEM in vivo. Our study suggests that mitochondrial GRIM-19 maybe a potential pathogenetic target for the SPEM pathogenesis, and its deficiency promotes SPEM through NLRP3/IL-33 pathway via a ROS-NRF2-HO-1-NF-кB axis. This finding not only provides a causal link between GRIM-19 loss and SPEM pathogenesis, but offers potential therapeutic strategies for the early prevention of intestinal GC.

Transformation of Chronic Atrophic Gastritis into Gastric Cancer and Prevention and Treatment： Based on Spleen Deficiency and Pathogen Stagnation / 中国实验方剂学杂志

Gastric ''inflammation-cancer'' transformation stars from inflammation and ends as gastric cancer （GC）， and the pathogenesis is still unclear. In China， GC features high morbidity and mortality and poor prognosis， influencing the quality of life and physical and mental health of patients. Therefore， it is of great significance to construct the prevention and treatment system for GC. Chronic atrophic gastritis （CAG） plays a key role in the occurrence， development， and outcome of gastric ''inflammation-cancer'' transformation. Modern therapies for CAG generally aim at eliminating causes and alleviating clinical symptoms， which show satisfactory short-term efficacy， but the reverse and recurrence are common. Based on the holistic view， syndrome differentiation-based treatment， and the ''inflammation-cancer'' transformation in modern medicine， traditional Chinese medicine emphasizes both prevention and treatment， with individualized therapies for CAG and GC to control the transformation. According to the pathogenesis of CAG-asthenia in origin and sthenia in superficiality and deficiency-excess in complexity， this study proposed the theory of spleen deficiency and pathogen stagnation in CAG， and believed spleen deficiency， pathogen， and stagnation are respectively the root cause of， the main factor of， and the key to ''inflammation-cancer'' transformation， respectively. Spleen deficiency and pathogen stagnation are closely related to the process of the transformation. For the treatment， the spleen-invigorating and pathogen-eliminating method should be used for invigorating the spleen to consolidate original Qi， improve the blood supply in stomach， and regulate immunity， and eliminating the pathogen to relieve stagnation， reduce the occurrence of non-controllable inflammation， and improve inflammatory micro-environment. As a result， the gastric inflammation is controlled at the early stage and the gastric ''inflammation-cancer'' transformation is blocked. The gastric mucosal lesions are blocked， delayed， or even reversed. This study provides a new idea in clinical diagnosis and treatment of CAG and in the prevention of GC.

Jian-Pi-Yi-Qi-Fang ameliorates chronic atrophic gastritis in rats through promoting the proliferation and differentiation of gastric stem cells.

Background: Jian-Pi-Yi-Qi-Fang (JPYQF) is a traditional Chinese medicine (TCM) herbal formula for treating chronic atrophic gastritis (CAG) in the clinic; however, its related mechanism remains unclear. The purpose of this study was to explore the potential mechanisms of JPYQF in treating CAG by examining proteins and genes related to the proliferation and differentiation of gastric stem cells and Wnt signaling. Methods: A CAG model was established in Sprague-Dawley (SD) rats which were induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and ranitidine. We randomly divided 25 CAG rats into 5 groups: the model group, positive drug group, low-dose group of JPYQF (JPYQF-L), middle-dose group of JPYQF (JPYQF-M), and high-dose group of JPYQF (JPYQF-H), with 5 rats of the same age classified into the control group. The body weight of rats was measured and their gastric morphology was visually assessed. Furthermore, pathological analysis of rat gastric tissue was performed. The expression levels of proteins and genes associated with the proliferation and differentiation of gastric stem cells and Wnt signaling were measured via immunohistochemistry and reverse transcription quantitative polymerase chain reaction (RT-qPCR). Results: Compared with the model group, treatment with JPYQF increased the body weight of the rats, and relieved the gastric atrophy and inflammation. Compared with the control group, the protein and messenger RNA (mRNA) expression levels of gastric stem cell proliferation and differentiation markers Lgr5, Sox2, Ki67, PCNA, Muc5AC, and Wnt signaling initiator Wnt3A and enhancer R-spondin-1 (Rspo1) were decreased in the model group. Treatment with JPYQF increased the protein and mRNA expression levels of these markers. Conclusions: The Wnt signaling of CAG rats may be in a low activation state, which inhibits the proliferation and differentiation of gastric stem cells, so that gland cells cannot be replenished in time to repair the damaged gastric mucosa. The TCM formula JPYQF could enhance Wnt signaling to promote the restricted proliferation and normal differentiation of gastric stem cells, thereby improving gastric mucosal atrophy in CAG rats, which provides a novel and robust theoretical basis for CAG treatment.

Zuojin Pill attenuates Helicobacter pylori-induced chronic atrophic gastritis in rats and improves gastric epithelial cells function in GES-1 cells.

ETHNOPHARMACOLOGICAL RELEVANCE: Zuojin pill (ZJP), a classical Chinese medicine formula, has been widely applied in Chinese clinical practice for the treatment of gastric injury such as acute gastric lesion, acute gastric mucosal injury, chronic unpredictable mild stress, gastroesophageal reflux disease, etc, thereby exerting anti-chronic atrophic gastritis (CAG) effects in traditional Chinese herbal medicine. AIM OF THE STUDY: This study was aimed to explore the therapeutic effects and molecular mechanisms of ZJP on Helicobacter pylori (H. pylori)-induced CAG based on the comprehensive approaches. MATERIALS AND METHODS: Sprague-Dawley rats were infected with H. pylori for 8 weeks to establish CAG model. Then, rats in the ZJP groups received doses of 0.63, 1.26, and 2.52 g/kg ZJP for 4 weeks. Therapeutic effects of ZJP on serum indices and the histopathology of the gastric were analyzed in vivo. Moreover, GES-1 cells were infected with H. pylori to establish gastric epithelial cell injury model in vitro. Cell viability and gastric epithelial cell morphology were detected by a high-content screening (HCS) assay. Furthermore, the relative mRNA and protein expression of JMJD2B/COX-2/VEGF axis and HMGB1/NF-κB signaling pathway in vivo and in vitro were determined by RT-PCR and Western Blotting, respectively. RESULTS: The results showed that the therapeutic effects of ZJP on CAG rats were presented in down-regulation serum biochemical indices and alleviating histological damage of gastric tissue. ZJP could dose-dependently decrease the serum IL-6, MCP-1, PGE2, TNF-α, and VEGF level and significantly improved gastric tissue inflammatory lesions. Besides, ZJP has an effect on increasing cell proliferation of GES-1 cells, ameliorating H. pylori-induced gastric epithelial cell damage. It was found that ZJP has a down-regulating effect on inflammatory reaction and could inhibit the relative mRNA and protein expression of JMJD2B/COX-2/VEGF axis and HMGB1/NF-κB signaling pathway in vivo and in vitro, including JMJD2B, COX-2, VEGF, VEGFR1, and VEGFR2, which in turn reduced the damage of gastric mucosal cells. CONCLUSIONS: The results suggested that ZJP exerts therapeutic effects on H. pylori-induced CAG by inhibiting the JMJD2B/COX-2/VEGF axis and HMGB1/NF-κB signaling pathway. These findings deeply explained why ZJP could be used to treat CAG clinically and clarified its pharmacological effect and potential mechanism in the treatment of CAG.

Prevalence of chronic atrophic gastritis worldwide from 2010 to 2020: an updated systematic review and meta-analysis.

BACKGROUND: Gastric cancer ranks 4th in cancer incidence and ranks 2nd in leading to cancer-related deaths worldwide. The present study aimed to provide an updated overview of the prevalence of chronic atrophic gastritis (CAG), one of the precancerous lesions of gastric cancer, in the recent 10 years and its association with Helicobacter pylori (HP) infection. METHODS: A meta-analysis of follow-up studies worldwide in the recent 10 years was performed by systematically searching in Web of Science, PubMed, Cochrane, and Embase. RESULTS: A total of 14 studies were finally enrolled in the present meta-analysis. The pooled results showed that the prevalence of CAG was about 25% in the study population, and the risk of CAG was about 2.4-fold higher in HP-positive patients than in those who were HP negative. Subgroup analyses showed that both the prevalence of CAG and the risk of CAG in HP-positive patients were higher when infection was diagnosed by histology than by serology. CONCLUSIONS: The worldwide prevalence of CAG is still high, and HP infection remains an important risk factor for CAG. Future studies of large-scale are still in urgent need to further control the prevalence of CAG, so as to reduce the burden of gastric cancer.

Systematic review and meta-analysis based on the composition of risk factors of chronic atrophic gastritis under gastroscopy detection.

BACKGROUND: This meta-analysis explored the diagnostic value of gastroscopy in the diagnosis of patients with chronic atrophic gastritis (CAG). METHODS: The Chinese and English medical databases were searched using a combination of the following search terms: "gastroscope", "chronic atrophic gastritis", "endoscope", and "diagnose". The Review Manager 5.3 software was used for meta-analysis. RESULTS: A total of 10 articles were included. The funnel charts showed that the circles of some articles were basically symmetrical with the midline, suggesting that there was no publication bias and the conclusions are credible. There were 6 randomized controlled trials (RCTs) analyzing clinical symptoms [Chi2 =5.33; degree of freedom (df) =5; I2=6%; P=0.38] and tested the overall heterogeneity [Z=7.94; odds ratio (OR) =9.42; 95% confidence interval (CI): 5.42 to 16.39; P<0.01]. A total of 10 articles analyzed the efficacy of gastroscopy (Tau2 =2.96; Chi2 =70.00; df =9; I2=87%; P<0.01) and tested the overall heterogeneity (Z=4.38; OR =13.44; 95% CI: 4.20 to 42.98; P<0.01). A total of 8 articles analyzed the pathological efficacy (Chi2 =11.93; df =7; I2=41%; P=0.10) and tested the overall heterogeneity (Z=10.59; OR =13.36; 95% CI: 8.27 to 21.59; P<0.01). The combined sensitivity and the specificity were 69.34% (95% CI: 0.526 to 0.784) and 96.45% (95% CI: 0.785 to 0.952), respectively. The area under the receiver operating characteristic (ROC) curve (AUC) of the combined sensitivity and combined specificity was 0.759 and 0.846, respectively. DISCUSSION: The results of the GRADE quality assessment revealed that although the sample size of this meta-analysis was small, the research was of sufficient medium and high quality, and the included experiments were of relatively good quality.

Effect of Weiwei Tongtiao Decoction on Expression of IKKβ, Bcl-2 in CAG Precancerous Lesion Rats / 中国实验方剂学杂志

Objective:To investigate the effect of Weiwei Tongtiao decoction on gastric mucosal pathology and the expression level of inhibitor kappa B kinase <italic>β</italic>（IKK<italic>β</italic>） and B-cell lymphoma-2（Bcl-2）in rats with chronic atrophic gastritis （CAG） precancerous lesion. Method:SD rats were randomly divided into normal group， model group， positive drug Weifuchun group， Weiwei Tongtiao decoction high， medium and low dose treatment groups. The rat model of CAG precancerous lesion was prepared by <italic>N</italic>-methyl-<italic>N</italic>'-nitro-<italic>N</italic>-nitrosoguanidine （MNNG）compound modeling method. weiwei Tongtiao decoction high， medium and low dose treatment groups received intragastric administration of 24， 12， 6 g·kg^-1 Weiwei Tongtiao decoction respectively， while Weifuchun group received 0.45 g·kg^-1 Weifuchun suspension， once per day for 12 weeks. The pathological changes of gastric mucosa of rats were observed by hematoxylin-eosin（HE）staining， and the mRNA and protein levels of IKK<italic>β</italic> and Bcl-2 in gastric mucosa of rats were detected by Real-time quantitative polymerase chain reaction （Real-time PCR）， immunohistochemistry（IHC）and Western blot. Result:Compared with the normal group， 100% inherent gland atrophy， mild to severe intestinal metaplasia， and 25% low-grade intraepithelial neoplasia were observed under microscope in model group. All Weifuchun group and Weiwei Tongtiao decoction groups could improve the atrophy of gastric glands， moderate to severe intestinal metaplasia and pathological injury of low-grade intraepithelial neoplasia， especially at high dose group. Compared with the normal group， IKK<italic>β</italic>， Bcl-2 mRNA and protein expressions in the gastric mucosa of the model group were up-regulated （<italic>P</italic><0.01）. Compared with the model group， the mRNA and protein expressions of IKK<italic>β</italic> and Bcl-2 in gastric mucosa of rats in the Weifuchun group and the Weiwei Tongtiao decoction high， medium and low dose groups were down-regulated （<italic>P</italic><0.05，<italic>P</italic><0.01）， showing a dose-dependent relationship， and such levels in the Weiwei Tongtiao decoction high-dose intervention group were similar to those in normal group. Conclusion:Weiwei Tongtiao decoction can improve and even reverse gastric mucosa with CAG precancerous lesions in rats， and its intervention mechanism may be related to down-regulating the expressions of IKK<italic>β</italic> and Bcl-2 in gastric mucosa.

Effect and Mechanism of Banxia Xiexintang on Rats with Chronic Atrophic Gastritis Based on Keap1/Nrf2/ARE Signaling Pathway / 中国实验方剂学杂志

Objective:To explore the mechanism of Banxia Xiexintang （BXXX） in preventing and treating chronic atrophic gastritis （CAG） through Kelch-like ECH-associated protein 1 （Keap1）/nuclear factor erythroid 2-related factor 2 （Nrf2）/antioxidant response element （ARE） signaling pathway. Method:SD rats were divided into a normal group （<italic>n</italic>=12） and an experimental group for CAG model induction. The model rats were then randomly divided into a model group， a vatacoenayme （VG） group （60 mg·kg^-1）， and high- （280 mg·kg^-1）， medium- （140 mg·kg^-1）， and low-dose （70 mg·kg^-1） BXXX groups. The doses in the BXXX groups were equivalent to 28， 14， and 7 g·kg^-1 crude drugs. The rats in the normal group and the model group received distilled water at an equal volume， and those in the VG group and the BXXX groups were treated correspondingly by gavage. After 12 weeks of treatment， hematoxylin-eosin （HE） staining was carried out to observe pathological changes in the gastric mucosa of CAG rats. Western blot and real-time fluorescence-based quantitative PCR was used to detect the protein and mRNA expression levels of Nrf2， glutathione S-transferase （GST）， and NAD （P）H：quinone oxidoreductase 1 （NQO1） in the gastric mucosa of CAG rats. Result:Compared with the normal group， the model group showed increased protein and mRNA expression levels of Nrf2， NQO1， and GST in the gastric mucosa of the rats （<italic>P</italic><0.05）， atrophic gastric mucosa， and even intestinal metaplasia. The protein and mRNA expression levels of Nrf2， NQO1， and GST in the VG group and the high- and medium-dose BXXX groups were lower than those in the model group （<italic>P</italic><0.05）， and gastric mucosa atrophy and intestinal metaplasia were significantly improved， especially in the high-dose BXXX group. However， the effect in the low-dose BXXX group was not significant. Conclusion:BXXX can blunt the transcriptional activity of Nrf2， shut down Nrf2 signaling pathway， and reduce the expression levels of NQO1 and GST to achieve normal oxidation-anti-oxidation balance， which may be one of its action mechanisms in the treatment of CAG.

[Effect of heat-sensitive moxibustion at "Zhongwan" (CV 12) on serum GH and PG in chronic atrophic gastritis rats].

OBJECTIVE: To observe the effect of heat-sensitive moxibustion at "Zhongwan" (CV 12) on serum growth hormone (GH) and pepsinogen (PG) in chronic atrophic gastritis (CAG) rats, and to explore the potential mechanism of heat-sensitive moxibustion for CAG. METHODS: A total of 66 male SD rats were randomized into a blank group (12 rats) and a model establishment group (54 rats). No intervention was given in the blank group. Rats in the model establishment group were intervented with compound pathogeny method for 12 weeks to establish CAG model, which were further divided into a model group (11 rats), a vitacoenzyme group (11 rats) and a moxibustion group (22 rats). In the moxibustion group, suspending moxibustion was applied at "Zhongwan" (CV 12) for 40 min. After the intervention of moxibustion, 0.9% sodium chloride solution was given by gavage (2 mL·kg-1·d-1). According to the changes of tail temperature, rats in the moxibustion group were divided into a heat-sensitive moxibustion group (11 rats) and a non-heat-sensitive moxibustion group (8 rats). The vitacoenzyme group was given vitacoenzyme as the same dose by gavage. The intervention was adopted once a day for 28 days. Changes of body weight were observed among the groups. Expressions of serum GH, PGⅠand PGⅡwere detected by ELISA, and the ratio of PGⅠand PGⅡ (PGR) was calculated. The morphological changes of gastric mucosa were observed by macroscopy and light microscope. RESULTS: ①After modeling, the body weight of rats in the model establishment group was lower than the blank group (P<0.01). Compared with the model group, the body weight of rats in the vitacoenzyme group, the heat-sensitive moxibustion group and the non-heat-sensitive moxibustion group was increased after intervention (P<0.05), and there were no significant differences among the intervention groups (P>0.05). ②Under macroscopy and light microscope, gastric tissue of rats after modeling showed dark red and pale gastric mucosa, lower plica and mucosal congestion. The glands of lamina propria were atrophied or disappeared with sparse and disordered arrangement, in which, lymphoid follicles and inflammatory cells could be observed. After intervention, morphology of gastric mucosa was improved in the vitacoenzyme group, the heat-sensitive moxibustion group and the non-heat-sensitive moxibustion group. ③Compared with the blank group, the serum levels of GH, PGⅠ, PGⅡ and PGR were decreased in the model group (P<0.05, P<0.01). Compared with the model group, the serum levels of GH, PGⅠand PGⅡwere increased in the vitacoenzyme group, the heat-sensitive moxibustion group and the non-heat-sensitive moxibustion group (P<0.05, P<0.01), the levels of PGR were increased without statistical difference (P>0.05). Compared with the vitacoenzyme group and the non-heat-sensitive moxibustion group, the serum levels of GH and PGⅠwere increased in the heat-sensitive moxibustion group (P<0.05). CONCLUSION: Heat-sensitive moxibustion at "Zhongwan" (CV 12) can improve the morphology of gastric mucosa in chronic atrophic gastritis rats, its mechanism may be related to the up-regulation of serum GH and PGⅠ.

Summary and Review of Animal Models for Chronic Atrophic Gastritis and Precancerous Lesions of Gastric Cancer / 中国实验方剂学杂志

Gastric cancer is a disease with high morbidity and mortality in the world, and also obtains attention in the global medicine. The occurrence of gastric cancer is a multi-stage and multi-factor process. A large number of epidemiological, pathological and clinical evidences have confirmed that the risk of gastric cancer in patients with chronic atrophic gastritis (CAG) is significantly correlated with the mortality of gastric cancer. Gastric mucosal atrophy, intestinal metaplasia (especially incomplete colonic metaplasia) and dysplasia are the main stages of precancerous lesions of precancerous lesions of gastric cancer (PLGC). Monitoring the condition of CAG patients, especially those with intestinal metaplasia and dysplasia, is of great significance for the discovery of early gastric cancer. CAG and PLGC are great significance in the pathological stage of gastric carcinogenesis. In recent years, more and more in-depth clinical and experimental studies have been carried out in this direction. So far, animal experiment is the main research way for CAG and PLGC disease, so it is very important to explore the modeling method. Choosing a stable and reliable model is the primary factor to study animal experiment. In view of the relationship between two diseases, this paper will summarize the methods of establishing animal models for CAG and PLGC in recent years, generally including chemical drug mutagenesis, physical stimulation, immune modeling, Helicobacter pylori infection replication and surgical modeling. Examples would be given for the application of various methods in the previous experiments, and the author would make a brief comment on the merits and demerits of these methods, which have been explored and successfully made by the author. This study would provide certain reference for the establishment and application of animal models in further CAG and PLGC experiments.

Influences of Chinese herbal compound Qinghuayin on serum IL-10 ,NO , GAS and plasma MTL in animal model of chronic atrophic gastritis in rats / 西安交通大学学报(医学版)

Objective To explore the effects of Chinese herbal compound Qinghuayin on the pathological changes of gastric mucosa and interleukin-10 (IL-10) ,nitric oxide (NO) ,gasmn (GAS) and motilin (MTL) in the serum in the animal model of chronic atrophic gastritis (CAG ) in rats .Methods We divided 53 Wistar rats randomly into blank control group (n=8) and CAG model group (n=45) ,and the animal model of CAG in rats was replicated by combination of disease and syndrome .After confirming the sampled rat model was successful built , the other 40 CAG rats in CAG model group were divided into model group ,vitacoenzyme tablet group ,low-dosage TMC group ,medium-dosage TMC group ,and high-dosage TMC group (each group n=8) .With the corresponding drug intervention to different rats for 30 days , the rats were executed . Then their blood was drawn from the abdominal aorta and the gastric tissue was taken to analyze the changes of serum IL-10 ,NO ,GAS and MTL concentrations and gastric mucosa pathology . Results Compared with blank control group , model group had various degrees of gastric mucosa atrophy ; decreased concentrations of serum IL-10 and GAS ; increased NO and MTL ( P<0 .01 ) .Compared with model group,Qinghuayin could improve gastric mucosa pathology in different degrees and increase the concentrations of IL-10 and GAS . Decrease the concentrations of NO and MTL( P<0 .05 or P<0 .01 ) . What's more. The curative effect in high-dosage TMC group was better( P<0. 01 ). Conclusion Chinese herbal compound Qinghuayin can effectively regulate the lopsided expressions of serum IL-10 . NO .GAS and MTL and reverse the pathological and histological changes in the gastric mucosa of CAG rats .

[Research progress on mechanism of acupuncture for chronic atrophic gastritis].

With the purpose of providing more references of acupuncture for chronic atrophic gastritis (CAG), the research achievements and action mechanism of acupuncture for CAG during past 20 years are summarized and analyzed. It is found that acupuncture could improve immune function, adjust central neural pathways, regulate gastroi-ntestinal hormone, increase stomach blood flow, regulate cytokines, increase gastric dynamics, control the gastric acid secretion, improve inflammatory response and regulate cell proliferation and apoptosis, which could strengthen gastric mucosa barrier. In addition, several problems and defects of related studies were pointed out, and reference and suggestion are provided for further clinical researches.

Research progress on mechanism of acupuncture for chronic atrophic gastritis / 中国针灸

With the purpose of providing more references of acupuncture for chronic atrophic gastritis (CAG), the research achievements and action mechanism of acupuncture for CAG during past 20 years are summarized and analyzed. It is found that acupuncture could improve immune function, adjust central neural pathways, regulate gastroi-ntestinal hormone, increase stomach blood flow, regulate cytokines, increase gastric dynamics, control the gastric acid secretion, improve inflammatory response and regulate cell proliferation and apoptosis, which could strengthen gastric mucosa barrier. In addition, several problems and defects of related studies were pointed out, and reference and suggestion are provided for further clinical researches.

Effects of traditional Chinese medicine Wei-Wei-Kang-Granule on the expression of EGFR and NF-KB in chronic atrophic gastritis rats.

Wei-Wei-Kang-Granule(WWKG) is a traditional Chinese medicine (TCM) preparation for the treatment of chronic atrophic gastritis (CAG). We examined the pathologic change and the effects of Wei-Wei-Kang-Granule (WWKG) on the expression of EGFR (epiderminal growth factor receptors) and NF-kB (nuclear transcription factor KappaB) in rats with chronic atrophic gastritis (CAG), and evaluated the possible mechanisms. Ninety rats were randomly divided into control group and four experimental groups. CAG rat models were induced by repeated stimulating experiments in the experimental groups. After modeled rats were intragastrically injected (i.g.) with WWKG at 6000mg/kg (large dose WWKG group), WWKG at 3000mg/kg (small dose WWKG group), San-Jiu-Wei-Tai-Granule(SJWTG) at 1600mg/kg(SJWTG group), and normal saline(0.9%)at 20ml/kg (model group and control group), respectively, once a day for 30 days. After 30 days, all rats were sacrificed and samples were taken from the sinus ventriculi and body of stomach. The gastric specimens were prepared for microscopic view with hematoxylin and eosin (H-E). The immunohistochemistry method was used to observe the expression of protein of EGFR and NF-kB in gastric tissue. The data were analyzed in pre-and post-treatment by computer image automatic analysis system. Immunohistochemistry detection showed that the average optical density of EGFR and NF-kB in antrum was lower in large and small dose WWKG groups than the model group (P<0.01). CAG in rats was related with the damage of barrier in gastric mucosa and the misbalance of cell proliferation and apoptosis. One of the mechanisms is perhaps to reduce the expressing of EGFR and NF-Kb in gastric mucosa.