Effect of jianpiyiwei capsule on gastric precancerous lesions in rats
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To evaluate the therapeutic effect of compound Chinese drugs, Jianpiyiwei capsule (JPYW) on gastric precancerous lesions in rats and to explore its mechanism of action.Model of gastric precancerous lesions was constructed in male Wistar rats: a metal spring was inserted and fixed through pyloric sphincter. One week after recovery, each rat was given 50-60 degrees hot paste containing 150 g/L NaCl 2 mL orally, twice a week for 15 weeks. Then 10 normal and 11 model rats were anaesthetized, after the measurement of gastric mucosa blood flow (GMBF), the rats were killed and the mucosal hexosamines and malonic dialdehyde (MDA) were measured. The morphological changes of gastric mucosa were observed macroscopically and microscopically, and by an automatic imaging analysis system. Other rats were treated with JPYW 1.5 g/kg.d(-1) or 4.5 g/kg.d(-1), or distilled water as negative control respectively (n=10 in each group). After 12 weeks, all the rats were examined as above.The gastric mucosa of model rats showed chronic atrophic gastritis with dysplasia and intestinal metaplasia (IM), GMBF and hexosamine content were reduced significantly and MDA was increased as compared to the normal group (P<0.01). After 12 weeks treatment, the pathological changes of the negative control group became worsened, while in JPYW treated groups the changes were modified with significant increase of GMBF and reduction of MDA, although the hexosamine concentration increased only mildly.JPYW increases GMBF and reduces MDA content in gastric mucosa and has therapeutic effects on gastric precancerous lesions.Keywords:
Atrophic gastritis
Intestinal metaplasia
Capsule
Metaplasia
The endoscopic atrophic border indicates the extent of atrophic gastritis. The aims of this study were to examine the relation of intestinal and diffuse types of gastric cancer to the atrophic border and to study the pathologic condition of the atrophic border.In 83 patients with gastric cancer the extent of atrophic gastritis was assessed macroscopically. In 46 patients gastric biopsy specimens were also taken, to compare the histologic features of gastritis proximal and distal to the atrophic border.Eighty-five per cent of gastric cancers (including 93% of intestinal type) occurred on the distal side of the atrophic border. Early diffuse gastric cancer arose closer to the atrophic border than intestinal-type cancer and was more likely to be sited proximal to it. Histologically, the grade of polymorphonuclear cell infiltration (inflammatory activity) and Helicobacter pylori density were significantly greater on the proximal side (P < 0.05), whereas the grades of glandular atrophy and intestinal metaplasia were significantly greater distally (P < 0.001).The atrophic border delineates the area of atrophic gastritis and intestinal metaplasia, and it is within the distal part of the stomach that gastric cancer occurs most frequently. Endoscopists should observe the distal side particularly carefully to identify early gastric cancer. The relationship of the two histologic types of cancer to areas of intestinal metaplasia and 'active' inflammation may have implications for the pathogenesis of cancer and, if so, for the potential protective effect of H. pylori eradication.
Atrophic gastritis
Intestinal metaplasia
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Objective To observe the curative effect of treatment to chronic atrophic gastritis(CAG)with gastric gastric dysplasia(Dys)or intestinal metaplasia(IM)according to syndrome differentiation.Methods 78 cases diagnosed as CAG with Dys or IM had been treated according to syndrome differientation for 3 months.Results The effective rate was 69.2%.The atrophic gland restored well,with Dys and(or)intestinal metaplasia notablely improved.Conclusion It is suggested that treatment according to syndrome differientation is effective for CAG,which can improve gastric dyaplasia and intestinal metaplasia.
Atrophic gastritis
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Objective To observe the curative effect in patients with chronic atrophic gastritis CAG with deficiency of both Qi and Yin and observe the expression of antioncogene protein P16 integral score before and after treatment. Methods The selected patients were suffered from chronic atrophic gastritis CAG with gastric mucous membrane dysplasia Dys and/or intestinal metaplasia IM diagnosed by endoscopy and pathologic examination. Sixty patients were randomly divided into treatment group and control group. The patients of treatment group were administrated with Shanwei invigorating the construction and function of stomach prescription and the patients of control group with heriacium tablet for six months. Result The overall effective rate of treatment group and control group was 90.00% and 55.67% respectively. There was an obvious difference between the treatment group and control group P0.01. In the treatment group some obvious improvements in the atrophy extent intestinal metaplasia and atypical hyperplasia were observed P0.05. The antioncogene protein P16 expression of treatment group was obviously higher than that of control group P0.05. Conclusion The Shanwei prescription has definite curative effect on chronic atrophic gastritis CAG with deficiency of both Qi and Yin and may reverse the pathologic change of the gastric mucous membrane on a certain extent by increasing the expression level of P16 protein probably.
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To explore the alteration and clinical significance of interleukin 23 (IL-23) and pepsinogen 1 (PG1) in the sera and tissues of patients with gastric diseases.The study collected the tissues of chronic superficial gastritis, chronic atrophic gastritis with intestinal metaplasia, gastric cancer as wells as the peripheral blood samples from the patients suffering from the three kinds of gastric diseases. Immunohistochemical staining was performed to detect IL-23 expression in the gastric involved tissues from these patients. The concentrations of serum PG1 were determined by time-resolved fluoroimmunoassay and the levels of serum IL-23 were detected by ELISA. The relationships between the serum IL-23 and PG1 in chronic atrophic gastritis with intestinal metaplasia tissues or gastric cancer tissues were analyzed by Pearson correlation analysis.Compared with the chronic superficial gastritis tissues, the expression of IL-23 significantly increased in chronic atrophic gastritis with intestinal metaplasia tissues and gastric cancer tissues, so did the serum IL-23. Nevertheless, the expression level of serum PG1 significantly decreased in chronic atrophic gastritis with intestinal metaplasia group and gastric cancer group. There was a negative correlation between IL-23 and PG1 in the chronic atrophic gastritis with intestinal metaplasia group or in gastric cancer group.Enhanced expression of IL-23 occurred in chronic atrophic gastritis with intestinal metaplasia tissue and gastric cancer tissue, and serum IL-23 had a negative correlation with PG1.
Atrophic gastritis
Intestinal metaplasia
Pepsin
Chronic gastritis
Metaplasia
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The clinical pathological characteristics of 3969 adult patients with chronic atrophic gastritis were retrospectively studied. The positivity of intestinal metaplasia and dysplasia in atrophic gastric specimens increased with age; however, H. pylori positivity and inflammatory activity decreased significantly with increased age. H. pylori infection was present in 21.01% of chronic atrophic gastritis patients, and 92.33% of the subjects with H. pylori infection were found to have simultaneous inflammatory activity. The intestinal metaplasia and dysplasia positivity markedly increased as the degree of gastric atrophy increased. In conclusion, the incidence of H. pylori infection decreased with age and correlated significantly with inflammatory activity in atrophic gastritis patients. The intestinal metaplasia and dysplasia positivity notably increased as the degree of gastric atrophy increased. Large population-based prospective studies are needed to better understand the progression of CAG.
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Objective To explore the mechanism of helicobacter pylori(Hp) infection in intestinal metaplasia of gastric mucosa and atrophic gastritis.Methods Totally 226 cases with Hp-positive were divided into treatment group(136 cases,Hp eradication therapy) and control group(130 cases,placebo therapy) randomly.To compare the degree of intestinal metaplasia,progression of atrophic gastritis,activity of telomerase,expression of Survivin mRNA between two groups.And compare pre and post treatment intragroups.Results It showed that higher expression of Survivin in intestinal metaplasia and atrophic gastritis.The Hp eradication therapy could reverse the intestinal metaplasia, release the progression of atrophic gastritis,reduce the expression of Survivin and inhibit the telomerase activity. It showed statistical significance in treatment group than control group(P0.01).Conclusion The Hp eradication therapy could help inhibit telomerase activity and expression of Survivin mRNA,to prevent the intestinal metaplasia.
Intestinal metaplasia
Atrophic gastritis
Survivin
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Helicobacter
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To analyze the Zhoushan residents atrophic gastritis risk factors.Gender,age,4 327 cases of atrophic gastritis HP infection,the degree of intestinal metaplasia,accompanied by dysplasia were analyzed.The result showed that atrophic gastritis incidence of male and female ratio 1:3;atrophy sex gastritis high risk age group in turn was 60 years of age group 40 years of age group 70 years of age group;intestinal metaplasia and high fat for 50 years of age group 60 years of age group 40 years of age group;HP infection male to female ratio 1:2.6;characteristics of the age of 50 years of age group 30 years of age group 40 years group;high incidence ages 30-39 years old atrophic gastritis with mild dysplasia,moderate dysplasia to high incidence of age 50-59.The island residents atrophic gastritis in women higher than men atrophic gastritis of the young people with more than mild dysplasia,was due to the high incidence of atrophic gastritis and diet,environment,gender and young people,HP infection was accompanied by related risk factors such as epithelial dysplasia.
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Objective To explore the relationship between different types of gastritis and gastric cancer.Methods The expression of p21 and p16 proteins in varioliform gastritis, non-atrophic gastritis, atrophic gastritis,and gastric cancer was detected by immunohistochemistry. The results were compared. Results The positive rate of p21 protein expression in non-atrophic gastritis, atrophic gastritis, varioliform gastritis, gastric cancer was 0, 22.5%,35.0%, 60.0%, respectively, which was significantly higher in varioliform gastritis than non-atrophic gastritis, but significantly lower than gastric cancer(P0.05). The positive rate of p16 protein expression in non-atrophic gastritis, atrophic gastritis, varioliform gastritis, gastric cancer was 90.0%, 50.0%, 45.0%, 17.5%, respectively, which was significantly lower in varioliform gastritis than non-atrophic gastritis, but significantly higher than gastric cancer(P0.01).No significant differences were noted between varioliform gastritis and atrophic gastritis. Conclusion Both p21 and p16 proteins may be involved in the evolution of varioliform gastritis to gastric cancer.
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ABSTRACT Background. This study evaluated the relationship between Helicobacter pylori infection, atrophic gastritis and intestinal metaplasia in Japan. Materials and Methods. This was a multicenter study performed in 21 centers in Japan. A total of 2455 individuals were enrolled. H. pylori status was determined by validated ELISAs. Atrophic gastritis was diagnosed by histology, endoscopy with Congo Red dye scattering or the Kimura‐Takemoto endoscopic classification. Results. Atrophic gastritis increased from 9.4% in those less than 20 years of age to > 70% in those aged 60 or older and was strongly associated with H. pylori infection. The overall prevalence of atrophic gastritis in H. pylori infection was 82.9% (1272/1534) compared with 9.8% (90/921) among uninfected (OR = 44.8; 95% CI = 34.7–57.8). Intestinal metaplasia was present in 43.1% (542/1258) of H. pylori positive persons compared with 6.2% (51/823) among the uninfected (OR = 11.5; 95% CI = 8.5–15.5). Atrophic gastritis in H. pylori positive Japanese was very high in the younger generation (38.5% in those aged 20 or less and 58.5% in those 21–30). Conclusions. Atrophic gastritis and intestinal metaplasia were strongly associated with H. pylori and not with aging. The fall in prevalence of H. pylori in Japan has not been associated with a corresponding fall in the prevalence of atrophic gastritis among those with H. pylori infection. The high prevalence of the precursor lesion, atrophic gastritis with intestinal metaplasia, among those with H. pylori infection suggests that the risk of development of early gastric cancer will continue to remain high in Japan.
Intestinal metaplasia
Atrophic gastritis
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Objective To study the significance of expression of hypoxia-inducible factor 1 alpha(HIF-1α) in gastric mucosal diseases. Methods Using tissue chip technique to creat tissue chip in 120 cases of vary gastric mucosal disease,and using S-P immunohistochemical methods to detect the expressions of HIF-1α in these tissue chips. Results The positive rates of HIF-1α was 28.3% in 120 tissue chips of gastric mucosal diseases. The positive rates of HIF-1α was 0, 10.0%, 40.0% and 63.3% in chronic superficial gastritis, chronic atrophic gastritis with intestinal metaplasia, chronic atrophic gastritis with dysplasia and intestinal type gastric cancer, respectively. The positive rates of HIF-1α of intestinal type gastric cancer and chronic atrophic gastritis with dysplasia were significantly higher than that in chronic superficial gastritis and chronic atrophic gastritis with intestinal metaplasia(P0.05). Conclusions The results demonstrate that HIF-1α is a good marker of gastric precancerous lesion. It is feasible to use of tissue chip for a rapid screen of massive tissue specimens clinically,and it is a high efficacy,economic and accurate method for delecting gastric precancerous lesion.
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