Cysteamine increases expression and activity of H^＋-K^＋-ATPase of gastric mucosal cells in weaning piglets

AIM: To determine the in vivo and in vivo effects of cysteamine (CS) on expression and activity of H(+)-K(+)-ATPase of gastric mucosal cells in weaning piglets. METHODS: Eighteen litters of newborn Xinhuai piglets were employed in the in vivo experiment and allocated to control and treatment groups. From 12 d of age (D12), piglets in control group were fed basal diet, while the treatment group received basal diet supplemented with 120 mg/kg CS. Piglets were weaned on D35 in both groups. Six piglets from each group (n = 6) were slaughtered on D28 (one week before weaning), D35 (weaning), D36.5, D38, D42, and D45 (36 h, 72 h, one week and 10 d after weaning), respectively. Semi-quantitative RT-PCR was performed to determine the levels of H(+)-K(+)-ATPase mRNA in gastric mucosa. H(+)-K(+)-ATPase activity in gastric mucosa homogenate was also determined. Gastric mucosal epithelial cells from piglets through primary cultures were used to further elucidate the effect of CS on expression and activity of H(+)-K(+)-ATPase in vivo. Cells were treated for 20 h with 0.001, 0.01, and 0.1 mg/mL of CS (n = 4), respectively. The mRNA expression of H(+)-K(+)-ATPase and somatostatin (SS) as well as the H(+)-K(+)-ATPase activity were determined. RESULTS: in vivo, both mRNA expression and activity of H(+)-K(+)-ATPase in gastric mucosa of control group exhibited a trend to increase from D28 to D45, reaching a peak on D45, but did not show significant age differences. Furthermore, neither the mRNA expression nor the activity of H(+)-K(+)-ATPase was affected significantly by weaning. CS increased the mRNA expression of H(+)-K(+)-ATPase by 73%, 53%, 30% and 39% on D28 (P = 0.014), D35 (P = 0.017), D42 (P = 0.013) and D45 (P = 0.046), respectively. In accordance with the mRNA expression, H(+)-K(+)-ATPase activities were significantly higher in treatment group than in control group on D35 (P = 0.043) and D45 (P = 0.040). In vivo, CS exhibited a dose-dependent effect on mRNA expression and activity of H+-K+-ATPase. Both H(+)-K(+)-ATPase mRNA expression and activity in gastric mucosal epithelial cells were significantly elevated after 20 h of exposure to the moderate (H(+)-K(+)-ATPase expression: P=0.03; H(+)-K(+)-ATPase activity: P = 0.014) and high concentrations (H(+)-K(+)-ATPase expression: P=0.017; H(+)-K(+)-ATPase activity: P = 0.022) of CS. Significant increases in SS mRNA expression were observed to accompany the elevation of H(+)-K(+)-ATPase expression and activity induced by the moderate (P = 0.024) and high concentrations (P = 0.022) of CS. Low concentration of CS exerted no effects either on expression and activity of H(+)-K(+)-ATPase or on SS mRNA expression in cultured gastric mucosal epithelial cells. CONCLUSION: No significant changes are observed in mRNA expression and activity of H(+)-K(+)-ATPase in gastric mucosa of piglets around weaning from D28 to D45. CS increases expression and activity of gastric H(+)-K(+)-ATPase in vivo and in vivo. SS is involved in mediating the effect of CS on gastric H(+)-K(+)-ATPase expression and activity in weaning piglets.     

Peroxynitrite induced decrease in Na^＋, K^＋-ATPase activity is restored by taurine

AIM: Peroxynitrite (ONOO-) is a powerful oxidant shown to damage membranes. In the present study, the effect of taurine on changes of liver plasma membrane Na+, K+-ATPase induced by ONOO- was investigated. METHODS: Liver plasma membrane was exposed to ONOO-with or without taurine. Na+, K+-ATPase activity and lipid peroxidation as thiobarbituric acid reactive substances (TBARS) levels were measured. RESULTS: Different concentrations of ONOO- (100, 200, 500, and 1 000 μmol/L) were found to decrease liver plasma membrane Na+, K+-ATPase activity significantly. The depletion of enzyme activity was not concentration dependent. Effects of different concentrations of taurine on liver plasma membrane Na+, K+-ATPase activity were also measured. Taurine did not cause any increase in enzyme activity. When plasma membranes were treated with 200 μmol/L ONOO- with different concentrations of taurine, a restoring effect of taurine on enzyme activity was observed. TBARS levels were also measured and taurine was found to decrease the elevated values. CONCLUSION: Taurine is observed to act as an antioxidant of ONOO- to decrease lipid peroxidation and thus affect liver plasma membrane Na+, K+-ATPase by restoring its activity.     

Prevalence of H pylori associated ‘high risk gastritis＇ for development of gastric cancer in patients with normal endoscopic findings

AIM: To investigate the prevalence of H pylori associated corpus-predominant gastritis (CPG) or pangastritis, severe atrophy, and intestinal metaplasia (IM) in patients without any significant abnormal findings during upper-GI endoscopy. METHODS: Gastric biopsies from 3548 patients were obtained during upper GI-endoscopy in a 4-year period. Two biopsies from antrum and corpus were histologically assessed according to the updated Sydney-System. Eight hundred and forty-five patients (mean age 54.8 +/- 2.8 years) with H pylori infection and no peptic ulcer or abnormal gross findings in the stomach were identified and analyzed according to gastritis phenotypes using different scoring systems. RESULTS: The prevalence of severe H pylori associated changes like pangastritis, CPG, IM, and severe atrophy increased with age, reaching a level of 20% in patients of the age group over 45 years. No differences in frequencies between genders were observed. The prevalence of IM had the highest increase, being 4-fold higher at the age of 65 years versus in individuals less than 45 years. CONCLUSION: The prevalence of gastritis featuring at risk for cancer development increases with age. These findings reinforce the necessity for the histological assessment, even in subjects with normal endoscopic appearance. The age-dependent increase in prevalence of severe histopathological changes in gastric mucosa, however, does not allow estimating the individual risk for gastric cancer development--only a proper follow-up can provide this information.     

Expression of cytokeratins in Helicobacter pylori -associated chronic gastritis of adult patients infected with cagA ＋ strains： An immunohistochemical study

AIM:To investigate the expression of differentcytokeratins(CKs)in gastric epithelium of adult patientswith chronic gastritis infected with Helicobacter pylori(Hpylori)cagA strains.METHODS:The expression of CK 7,8,18,19 and 20was studied immunohistochemically in antral gastricbiopsies of 84 patients.All the CKs were immunostainedin cagA H pylori gastritis(57 cases),non-H pylori gastritis(17 cases)and normal gastric mucosa(10 cases).RESULTS:In cagA H pylori gastritis,CK8 wasexpressed comparably to the normal antral mucosafrom surface epithelium to deep glands.Distributionof CK18 and CK 19 was unchanged,i.e.transmucosal,but intensity of the expression was different in foveolarregion in comparison to normal gastric mucosa.Cytokeratin 18 immunoreactivity was significantly higherin the foveolar epithelium of H pylori-positive gastritiscompared to both Hpylori-negative gastritis and controls.On the contrary,decrease in CK19 immunoreactivityoccurred in foveolar epithelium of H pylori-positive gastritis.In both normal and inflamed antral mucosawithout Hpylori infection,CK20 was expressed strongly/moderately and homogenously in surface epithelium andupper foveolar region,but in H pylori-induced gastritissignificant decrease of expression in foveolar regionwas noted.Generally,in both normal antral mucosa andH pylori-negative gastritis,expression of CK7 was notobserved,while in about half cagA H pylori-infectedpatients,moderate focal CK7 immunoreactivity of theneck and coiled gland areas was registered,especially inareas with more severe inflammatory infiltrate.CONCLUSION:Alterations in expression of CK 7,18,19 and 20 together with normal expression of CK8 occurin antral mucosa of H pylori-associated chronic gastritisin adult patients infected with cagA strains.Alterationsin different cytokeratins expression might contribute toweakening of epithelial tight junctions observed in Hpylori-infected gastric mucosa.     

Effects of L-arginine on serum nitric oxide, nitric oxide synthase and mucosal Na^＋-K^＋-ATPase and nitric oxide synthase activity in segmental small-bowel autotransplantation model

AIM:To explore a simple method to create intestinal autotransplantation in rats and growing pigs and to investigate the effect of L-arginine supplementation on serum nitric oxide (NO), nitric oxide synthase (NOS) and intestinal mucosal NOS and Na+-K+-ATPase activity during cold ischemia-reperfusion (IR) in growing pigs. METHODS: In adult Wistar rat models of small bowel autotransplantation, a fine tube was inserted into mesenteric artery via the abdominal aorta. The superior mesenteric artery and vein were occluded. Isolated terminal ileum segment was irrigated with Ringer's solution at 4℃ and preserved in the same solution at 0-4℃ for 60 min. Then, the tube was removed and reperfusion was established. In growing pig models, a terminal ileum segment, 50 cm in length, was isolated and its mesenteric artery was irrigated via a needle with lactated Ringer's solution at 4℃. The method and period of cold preservation and reperfusion were described above. Ten white outbred pigs were randomly divided into control group and experimental group. L-arginine (150 mg/kg) was continuously infused for 15 min before reperfusion and for 30 min after reperfusion in the experimental group. One, 24, 48, and 72 h after reperfusion, peripheral vein blood was respectively collected for NO and NOS determination. At the same time point, intestinal mucosae were also obtained for NOS and Na+-K+-ATPase activity measurement. RESULTS: In adult rat models, 16 of 20 rats sustained the procedure, three died of hemorrhage shock and one of deep anesthesia. In growing pig models, the viability of small bowel graft remained for 72 h after cold IR in eight of 10 pigs. In experimental group, serum NO level at 1 and 24 h after reperfusion increased significantly when compared with control group at the same time point (152.2±61.4μmol/L /s60.8±31.6μmol/L, t=2.802, P=0.02<0.05; 82.2±24.0μmol/L vs 54.0±24.3μmol/L, t=2.490, P=0.04<0.05). Serum NO level increased significantly at 1 h post-reperfusion when compared with the same group before cold IR, 24 and 48 h post-reperfusion (152.2±61.4μmol/L vs 75.6±16.2μmol/L,t=2.820, P=0.02<0.05,82.2±24.0μmol/L,t=2.760, P= 0.03<0.05, 74.2±21.9μmol/L, t=2.822, P= 0.02<0.05). Serum NOS activity at each time point had no significant difference between two groups. In experimental group, intestinal mucosal NOS activity at 1 h post-reperfusion reduced significantly when compared with pre-cold IR (0.79±0.04 U/mg vs 0.46±0.12 U/mg, t = 3.460, P= 0.009<0.01). Mucosal NOS activity at 24, 48, and 72 h post-reperfusion also reduced significantly when compared with pre-cold IR (0.79±0.04 U/mg vs 0.57±0.14 U/mg, t= 2.380, P=0.04 <0.05, 0.61±0.11 U/mg, t= 2.309, P = 0.04<0.05, 0.63±0.12U/mg, t = 2.307, P= 0.04<0.05). In control group, mucosal NOS activity at 1 and 24 h post-reperfusion was significantly lower than that in pre-cold IR (0.72±0.12 U/mg vs 0.60±0.07 U/mg, t= 2.320, P= 0.04<0.05, 0.58±0.18 U/mg, t=2.310, P= 0.04<0.05). When compared to the normal value, Na+-K+-ATPase activity increased significantly at 48 and 72 h post-reperfusion in experimental group (2.48±0.59μmol/mg vs 3.89±1.43μmol/mg, t=3.202, P= 0.04<0.05, 3.96±0.86μmol/mg, t=3.401, P= 0.009 <0.01) and control group (2.48±0.59μmol/mg vs 3.58±0.76 μmol/mg, t=2.489, P= 0.04<0.05, 3.67±0.81μmol/mg, t= 2.542, P= 0.03<0.05). CONCLUSION: This novel technique for intestinal autotransplantation provides a potentially consistent and practical model for experimental studies of graft cold preservation. L-arginine supplementation during cold IR may act as a useful adjunct to preserve the grafted intestine.     

High concentrations of human β-defensin 2 in gastric juice of patients with Helicobacter pyloriinfection

AIM: Human beta-defensin (HBD)-1 and HBD-2 are endogenous antimicrobial peptides. Unlike HBD-1, the HBD-2 expression is augmented by Helicobacter pylori (H pylori). We sought to determine HBD-1 and HBD-2 concentrations in gastric juice during H pylori infection. METHODS: HBD-1 and HBD-2 concentrations were measured by radioimmunoassay in plasma and gastric juice of 49 H pylori-infected and 33 uninfected subjects and before and after anti-H pylori treatment in 13 patients with H pylori-associated gastritis. Interleukin (IL)-1beta and IL-8 concentrations in gastric juice were measured by enzyme-linked immunosorbent assay (ELISA). Histological grades of gastritis were determined using two biopsy specimens taken from the antrum and corpus. Reverse phase high performance liquid chromatography (RP-HPLC) was used to identify HBD-2. RESULTS: HBD-2 concentrations in gastric juice, but not in plasma, were significantly higher in H pylori-positive than -negative subjects, albeit the post-treatment levels were unchanged. Immunoreactivity for HBD-2 was exclusively identified in H pylori-infected mucosa by RP-HPLC. HBD-2 concentrations in gastric juice correlated with histological degree of neutrophil and mononuclear cell infiltration in the corpus. IL-1beta levels correlated with those of IL-8, but not HBD-2. Plasma and gastric juice HBD-1 concentrations were similar in H pylori-infected and uninfected subjects. CONCLUSION: Our results place the beta-defensins, especially HBD-2, in the front line of innate immune defence. Moreover, HBD-2 may be involved in the pathogenesis of H pylori-associated gastritis, possibly through its function as immune and inflammatory mediator.     

Evaluation of the use of rapid urease test： Pronto Dry to detect H pylori in patients with dyspepsia in several cities in Indonesia

INTRODUCTION H pylori is a microaerophylic, gram negative, slowly growing, and pathogenic bacterium which produces urease enzyme[1]. H pylori may cause chronic gastritis and predispose to gastric and duodenal ulcer. Recently, H pylori has been classified …     

Effect of Qingyitang on activity of intracellular Ca^2＋-Mg^2＋-ATPase in rats with acute pancreatitis

AIM: To study the change of intracellular calcium-magnesium ATPase (Ca(2+)-Mg(2+)-ATPase) activity in pancreas, liver and kidney tissues of rats with acute pancreatitis (AP), and to investigate the effects of Qingyitang (QYT) (Decoction for clearing the pancreas) and tetrandrine (Tet) and vitamin E (VitE) on the activity of Ca(2+)-Mg(2+)-ATPase. METHODS: One hundred and five Sprague-Dawley rats were randomly divided into: normal control group, AP group, treatment group with QYT (1 ml/100 g) or Tet (0.4 ml/100 g) or VitE (100 mg/kg). AP model was prepared by a retrograde injection of sodium taurocholate into the pancreatic duct. Tissues of pancreas, liver and kidney of the animals were taken at 1 h, 5 h, 10 h respectively after AP induction, and the activity of Ca(2+)-Mg(2+)-ATPase was studied using enzyme-histochemistry staining. Meanwhile, the expression of Ca(2+)-Mg(2+)-ATPase of the tissues was studied by RT-PCR. RESULTS: The results showed that the positive rate of Ca(2+)-Mg(2+)-ATPase in AP group (8.3%, 25%, 29.2%) was lower than that in normal control group (100%) in all tissues (P<0.01), the positive rate of Ca(2+)-Mg(2+)-ATPase in treatment group with QYT (58.3%, 83.3%, 83.3%), Tet (50.0%, 70.8%, 75.0%) and VitE (54.2%, 75.0%, 79.2%) was higher than that in AP group (8.3%, 25.0%, 29.2%) in all tissues (P<0.01). RT-PCR results demonstrated that in treatment groups Ca(2+)-Mg(2+)-ATPase gene expression in pancreas tissue was higher than that in AP group at the observing time points, and the expression at 5 h was higher than that at 1 h. The expression of Ca(2+)-Mg(2+)-ATPase in liver tissue was positive, but without significant difference between different groups. CONCLUSION: The activity and expression of intracellular Ca(2+)-Mg(2+)-ATPase decreased in rats with AP, suggesting that Ca(2+)-Mg(2+)-ATPase may contribute to the occurrence and development of cellular calcium overload in AP. QYT, Tet and VitE can increase the activity and expression of Ca(2+)-Mg(2+)-ATPase and may relieve intracellular calcium overload to protect the tissue and cells from injuries.     

CagA＋ H pylori infection is associated with polarization of T helper cell immune responses in gastric carcinogenesis

AIM:To characterize the immune responses including local and systemic immunity induced by infection with H pylori,especially with CagA+ H pylori strains and the underlying immunopathogenesis. METHODS:A total of 711 patients with different gastric lesions were recruited to determine the presence of H pylori infection and cytotoxin associated protein A (CagA),the presence of T helper (Th) cells and regulatory T (Treg) cells in peripheral blood mononuclear cells (PBMCs),expression of plasma cytokines,and RNA and protein expression of IFN-γ and IL-4 in gastric biopsies and PBMCs were determined by rapid urease test,urea 14C breath test,immunoblotting test,flow cytometry ,real time RT-PCR and immunohistochemistry. RESULTS:Of the patients,629 (88.47%) were infected with H pylori ; 506 (71.16%) with CagA+ and 123 (17.30%) with CagA- strains. Among patients infected with CagA+ H pylori strains,Th1-mediated cellular immunity was associated with earlier stages of gastric carcinogenesis,while Th2-mediated humoral immunity dominated the advanced stages and was negatively associated with an abundance of Treg cells. However,there was no such tendency in Th1/Th2 polarization in patients infected with CagA- H pylori strains and those without H pylori infection. CONCLUSION:Polarization of Th cell immune responses occurs in patients with CagA+ H pyloriinfection,which is associated with the stage and severity of gastric pathology during the progression of gastric carcinogenesis. This finding provides further evidence for a causal role of CagA+ H pylori infection in the immunopathogenesis of gastric cancer.     

Expression of nuclear factor-kappa B and target genes in gastric precancerous lesions and adenocarcinoma： Association with Helicobactor pylori cagA （＋） infection

AIM:To examine the expression of nuclear factor kappaB (NF-κB) and its target genes in intestinal metaplasia (IM),dysplasia (DYS) and gastric carcinoma (GC) infected with Helicobacter pylori (H pylori) and to investigate the mechanism underlying Hpyloricytotoxin associated gene A(cag A) infection leading to gastric adenocarcinoma.METHODS: Expressions of NF-κB/p65 and its target genes:c-myc, cyclinD1 and bcl-xl were immunohistochemically examined in 289 cases of gastric biopsy and resection specimens from patients with IM, DYS and GC infected with H pylori. H pylori in the above mentioned tissues was detected by Warthin-Starry stain and rapid urease tests.IgG antibody to cagA in sera of the patients was measured by ELISA.RESULTS:The positive rates of NF-κB/p65 were significantly higher in groups with cagA of IMI-Ⅱ(28/33), IM III(48/52),DYSI(27/31), DY5 Ⅱ-Ⅲ(28/32), GC(35/40) than in groups without cagA of IMI-Ⅱ(4/17), IMⅢ(3/20), DYSI(3/20),DYSⅡ-Ⅲ(6/21), GC(10/23). The expressions of c-myc,cyclinD1, and bcl-xl were significantly higher in groups with cagA of IM Ⅲ(47/52, 49/52, 46/52), DYSⅡ-Ⅲ(29/32, 26/32,25/32) than in groups without cagA of IM Ⅲ(8/20, 7/20,5/20), DYSⅡ-Ⅲ(10/21, 8/21, 3/21), which were in conformity with the expression of NF-κB in IM Ⅲ, and DYSⅡ-Ⅲ. Asignificantly higher expression level of NF-κB/p65, c-myc,cyclinD1 and bcl-xl was detected in intestinal type GC(27/28,18/28, 22/28, 24/28) than in diffuse type GC(8/12, 3/12,3/12, 6/12), respectively.CONCLUSION: There may be two different molecular mechanisms in the occurrence of intestinal and diffuse type gastric carcinomas. Intestinal type gastric carcinoma is strongly associated with high expression of c-myc, cyclinD1 and bcl-xl through NF-κB/p65 activated by Hpylori cagA.Inhibiting the activity of NF-κB is an effective and promising way to prevent intestinal type gastric carcinoma.     

慢性胃炎、胃癌组织中幽门螺杆菌基因分型的临床研究

目的 探讨幽门螺杆菌(HP)基因分型与慢性胃炎、胃癌的关系。方法 应用PCR—RFLP方法对36例慢性胃炎及45例胃癌组织中的幽门螺杆菌菌株进行检测。并用HindⅡ酶切尿毒酶B(UreB)扩增基因产物进行多态性分析。结果 36例慢性胃炎HP阳性24例(66．7％),45例胃癌组织中HP阳性23例(51．1％)。二者差异无显著性。47例HP阳性标本均显示不同的RFLP图谱。胃癌组织中未发现特异性条带。结论 慢性胃炎、胃癌与HP感染密切相关。HP基因具有多态性,HP菌株存在基因型差异。PCR—RFLP方法可对HP菌株进行鉴定并将其分型。     

Effects of bile reflux on gastric mucosal lesions in patients with dyspepsia or chronic gastritis

AIM: To investigate the influences of bile reflux on profiles of gastric mucosal lesions in patients with dyspepsia or chronic gastritis. METHODS: A total of 49 patients diagnosed with dyspepsia and chronic gastritis underwent 24-h ambulatory and simultaneous monitoring of intragastric bilirubin absorbance and pH values, and then they were divided into bile reflux positive group and bile reflux negative group. Severity of pathological changes in gastric mucosa including active inflammation, chronic inflammation, intestinal metaplasia, atrophy and dysplasia as well as Helicobacter pylori (H pylori) infection at the corpus, incisura and antrum were determined respectively according to update Sydney system criteria. The profiles of gastric mucosal lesions in the two groups were compared, and correlations between time-percentage of gastric bilirubin absorbance >0.14 and severity of gastric mucosal lesions as well as time-percentage of gastric pH >4 were analyzed respectively. RESULTS: Thirty-eight patients (21 men and 17 women, mean age 44.2 years, range 25-61 years) were found existing with bile reflux (gastric bilirubin absorbance >0.14) and 11 patients (7 men and 4 women, mean age 46.2 years, range 29-54 years) were bile reflux negative. In dyspepsia patients with bile reflux, the mucosal lesions such as active inflammation, chronic inflammation, intestinal metaplasia, atrophy or H pylori infection in the whole stomach, especially in the corpus and incisura, were significantly more severe than those in dyspepsia patients without bile reflux. Moreover, the bile reflux time was well correlated with the severity of pathological changes of gastric mucosa as well as H pylori colonization in the near-end stomach, especially in the corpus region. No relevance was found between the time of bile reflux and pH >4 in gastric cavity. CONCLUSION: Bile reflux contributes a lot to mucosal lesions in the whole stomach, may facilitate H pylori colonization in the corpus region, and has no influence on acid-exposing status of gastric mucosa in patients with dyspepsia or chronic gastritis.     

Expression of mutant type-p53 products in H pylori-associated chronic gastritis

AIM:To investigate the mutation of p 53 immuno-histochemically in non-tumorous gastric mucosa with H pylori infection before and after H pylori eradication therapy.METHODS:53 subjects(36 male,17 female,mean age ± SEM,57.1 ± 12.1)undergoing endoscopic examination were included in this study.42 of 53 patients were H pylori-positive,and 11 were H pylori-negative.All H pylori-positive patients had successful eradication therapy.Biopsy specimens were taken from five points of the stomach,as recommended by the updated Sydney system.Immunohistochemical studies were performed by using primary antibodies against p53(DO-7 and PAb240).RESULTS:p53(DO-7 and PAb240)immunoreactivity was shown in the neck region of the gastric pits,however,quite a few cells were found to be immunopositive for p 53(PAb240)in the H pylori-infected gastric mucosa.The proportion of patients immunopositive for p 53(PAb240)was significantly reduced 6 mo after eradication [28/42(66.7%)to 6/42(14.3%)](P < 0.05),while the biopsies taken from H pylori-negative patients showed no immunoreactivity for p53(PAb240).p53(PAb240)-positive patients were divided into two groups by the number of positive cells detected:one with more than six positive cells per 10 gastric pits(group A,n = 12),and the other with less than five positive cells per 10 gastric pits(group B,n = 30).Atrophy scores in group A were significant higher than those in group B at the greater curvature of the antrum(group A:2.00 ± 0.14 vs group B:1.40 ± 0.15,P = 0.012),the lesser curvature of the corpus(group A:2.00 ± 0.21 vs group B:1.07 ± 0.23,P = 0.017),and the greater curvature of the corpus(group A:1.20 ± 0.30vs group B:0.47 ± 0.21,P = 0.031).Group A showed significant higher intestinal metaplasia scores than group B only at the lesser curvature of the antrum(group A:2.10 ± 0.41 vs group B:1.12 ± 0.29,P = 0.035).CONCLUSION:H pylori-associated chronic gastritis expressed the mutant-type p53,which was significantly associated with more severe atrophic and metaplastic changes.H pylori eradication led to a significant reduction in the expression of the mutant-type p53.It is considered that H pylori-infected chronic gastritis is associated with a genetic instability that leads to gastric carcinogenesis,and H pylori eradication may prevent gastric cancer.     

幽门螺杆菌相关性胃炎患者血清胃蛋白酶原检测的临床价值

背景幽门螺杆菌(Helicobacter pylori,Hp)可引起胃黏膜细胞的慢性炎症,并诱导胃黏膜细胞分泌胃蛋白酶原,导致血液中胃蛋白酶原含量的变化。目的探讨Hp相关性胃炎患者血清胃蛋白酶原含量变化的临床价值。方法对经胃镜和病理证实为浅表性胃炎和萎缩性胃炎的患者按照Hp阳性及阴性进行分组,采用ELISA法对其血清PGⅠ、PGⅡ含量进行检测,血清Hp-IgG抗体采用定性分析法。结果无论浅表性胃炎或萎缩性胃炎,Hp阳性组同阴性组之间比较,差异均有显著意义(P0.05);在萎缩性胃炎组中,血清PGⅠ含量较浅表性胃炎组者中明显降低,两者相比差异有显著意义(P0.05)。结论Hp感染慢性胃炎患者血清中PGⅠ、PGⅡ含量明显增加,PGⅠ含量的变化可以反映胃黏膜病变的程度。     

慢性多灶萎缩性胃炎患者胃酸分泌与幽门螺杆菌感染及血清胃泌素的关系

目的 研究慢性多灶萎缩性胃炎(BAG)胃酸分泌与幽门螺杆菌(Hp)感染及血清胃泌素的关系.方法 将200例确诊的慢性胃炎患者根据病理结果分为轻度、中度、重度BAG组及对照组(非萎缩性胃炎组),监测各组患者24小时胃内pH值的变化情况,并检测其幽门螺杆菌及血清胃泌素的含量,各组间进行比较.结果 (1)150例BAG患者中,Hp感染阳性率70%,随着胃粘膜萎缩程度的加重,Hp感染阳性率逐渐上升;(2)各组间血清胃泌素值比较:轻度萎缩组与非萎缩性胃炎组比较差异无显著性(P＞0.05),其余各组问比较差异有显著性(P＜0.05;(3)各组pH值分析结果:BAC胃黏膜轻度萎缩时,pH≤2时间百分比较非萎缩性胃炎组升高,pH＞4时间百分比及pH平均值、pH中位值均较非萎缩性胃炎组降低,中度及重度萎缩时pH≤2时间百分比逐渐降低,pH＞4时间百分比及pH平均值、pH中位值逐渐升高.结论 BAG的发生与Hp感染有关,胃粘膜萎缩程度与Hp感染的严重程度有关;BAG胃黏膜轻度萎缩时,血清胃泌素含量无明显变化;中、重度萎缩时,血清胃泌素含量降低;BAc胃黏膜轻度萎缩时,胃酸分泌增多;随着胃黏膜萎缩程度的加重,胃酸分泌逐渐减少.     

Influence of H pylori on plasma ghrelin in patients without atrophic gastritis

AIM:To determine the association between H pylori infection and serum ghrelin levels in patients without atrophic gastritis.METHODS:Fifty consecutive patients(24 males and 26 females)with either H pylori-positive gastritis(n = 34)or H pylori-negative gastritis(n = 16)with normal gastric acid secretion determined by 24-h pHmetry and without atrophic gastritis in histopathology were enrolled in this study.Thirty-four H pylori-infected patients were treated with triple therapy consisting of a daily regimen of 30 mg lansoprazole bid,1 g amoxicillin bid and 500 mg clarithromycin bid for 14 d,followed by an additional 4 wk of 30 mg lansoprazol treatment.H pylori infection was eradicated in 23 of 34(67.6%)patients.H pylori-positive patients were given eradication therapy.Gastric acidity was determined via intragastric pH catethers.Serum ghrelin was measured by radioimmunoassay(RIA).RESULTS:There was no signifficant difference in plasma ghrelin levels between H pylori-positive and H pylori-negative groups(81.10 ± 162.66 ng/L vs 76.51 ± 122.94 ng/L).In addition,there was no significant difference in plasma ghrelin levels and gastric acidity levels measured before and 3 mo after the eradication therapy.CONCLUSION:H pylori infection does not influence ghrelin secretion in patients with chronic gastritis without atrophic gastritis.     

Alteration of sister chromatid exchange frequencies in gastric cancer and chronic atrophic gastritis patients with and without H. pylori infection

AIM： To determine, by counting sister chromatid exchange （SCE） frequencies, whether genetic impairment and DNA damage have an effect on the pathogenesis of gastric cancer （GC）. METHODS： Analysis of SCE is a cytogenetic technique used to show DNA damage as a result of an exchange of DNA fragments between sister chromatids. We analyzed SCE frequency in 24 patients with GC, 26 patients with chronic atrophic gastritis （CAG）, and 15 normal controls. The presence of H pylori was confirmed by urease test, toluidine-blue stain and hematoxylin-eosin stain. RESULTS： SCE was significantly increased in H pylori- negative GC patients, and in H pylori-negative CAG patients compared with controls （7.41 ± 1.36 and 6.92 ± 1.20, respectively, vs 5.54 ± 0.8, P 〈 0.001）. There was no difference in the SCE frequency between H pylori- negative GC patients and H pylori-negative CAG patients （P 〉 0.05）. On other hand, the SCE frequencies in H pylori-positive GC patients were higher than those in H pylori-positive CAG patients （9.20 ± 0.94 vs 7.93 ± 0.81, P 〈 0.01）. Furthermore, H pylori-positive GC patients had a higher SCE frequency than H pylori- negative GC patients （9.20 ± 0.94 vs 7.41 ± 1.36, P 〈 0.001）. Similarly, a significant difference was detected between H pylori-positive CAG patients and H pylori-negative CAG patients （7.93 ± 0.81 vs 6.92 ± 1.20, P 〈 0.05）. CONCLUSION： We suggest the increased SCE in patients reflects a genomic instability that may be operative in gastric carcinogenesis.     

幽门螺杆菌感染慢性胃炎患者红细胞免疫功能变化的研究

目的　探讨红细胞免疫在幽门螺杆菌感染慢性胃炎发病机制中的作用。方法　对 91例 Hp(+)慢性胃炎患者 [Hp(+)组 ],给予抗 Hp三联 +胃动力药治疗 2周 ;2 2例 Hp(- )慢性胃炎患者 ,给予胃粘膜保护剂 +胃动力药治疗 2周。治疗前及治疗结束后 2个月分别进行胃镜及 Hp检测 ,并测定两组红细胞免疫功能及胃粘膜屏障功能。结果　治疗前 Hp(+)组与 Hp(- )组红细胞免疫功能比较 ,前者 RBC- C3b RR偏低 ,而 RBC- ICR偏高 ,胃粘膜屏障功能较差 (P<0 .0 5 ) ;治疗后两组间无显著性差异 (P>0 .0 5 )。结论　慢性胃炎患者红细胞免疫功能降低 ,其与 Hp感染存在相关性。     

胆汁反流性胃炎患者幽门螺杆菌感染及其胃粘膜病理学表现研究*

目的 探讨胆汁反流性胃炎（BRG）患者幽门螺杆菌（Hp）感染及其胃粘膜病理学变化。方法 我院诊治的BRG患者618例和无胆汁反流的慢性浅表性胃炎（CSG）患者1486例,采用¹⁴C-尿素呼气试验、血清抗-Hp抗体检测和对组织切片行硼酸亚甲蓝染色三种方法对受试者进行Hp感染诊断,常规行胃镜检查,参照新悉尼系统标准,将组织学上胃黏膜慢性炎性反应、炎性反应活动性、萎缩和肠上皮化生的严重程度分为无、轻、中和重4个等级。结果 BRG患者Hp感染率为32.7%（202/618）,而CSG组患者为40.6%（603/1486）,两组间无显著性差异（P>0.05）;在202例Hp阳性的BRG患者中,胃粘膜轻、中、重度炎症反应发生率分别为10.9%、61.4%和27.7%,显著重于416例Hp阴性患者的40.4%、51.7%和7.9%（P<0.05）,胃粘膜淋巴滤泡形成、肠化生和活动性炎症发生率分别为15.4%、5.4%和16.8%,也显著重于Hp阴性患者的2.7%、10.8%和0.7%（P<0.05）;603例Hp阳性的CSG患者胃粘膜轻、中、重度炎症反应发生率分别为29.2%、59.4%和11.5%,与883例Hp阴性患者的34.1%、54.0%和11.9%比,无显著性差异（P>0.05）,胃粘膜淋巴滤泡形成、肠化生和活动性炎症发生率分别为10.4%、1.8%和8.5%,与Hp阴性患者的7.8%、1.0%和5.0%比,也无显著性差异（P>0.05）;观察胃粘膜病理学轻度、中度和重度炎症情况发现,117例内镜下胃粘膜III级BRG患者炎症程度显著重于200例I级或301例II级患者（P<0.05）。结论 BRG患者无论是胃镜下表现还是胃粘膜组织病理学变化都存在明显的病变,胆汁反流和Hp感染是引起胃粘膜炎症反应的重要因素。