胃癌中幽门螺杆菌感染与原癌基因c—met表达及预后研究

目的　研究幽门螺杆菌(Hp)感染的胃癌(GC)组织中c-met表达及(Hp)感染对胃癌预后的影响。方法　经病理证实,不同病变胃粘膜145例以免疫组化检测c-met基因表达,以W-S法及快速尿素酶试验检测(Hp)感染。结果　在浅表性胃炎(CSG)、萎缩肠化生胃炎(CAG+IM)、异型增生(DYS)、早期GC和进展期GC中,c-met基因表达率分别为25.53%,51.28%,61.54%,66.67%和68.42%,CAG+IM、DYS、GC均显著高于CSG(P＜0.05)。肠型胃癌c-met阳性表达与(Hp)感染密切相关。CAG+IM,DYS和GC组c-met阳性表达(Hp)感染者明显高于阴性组。(Hp)阳性者5年生存期显著短于(Hp)阴性者。结论　(Hp)感染和c-met表达与胃粘膜增殖和恶化有关,前者也与胃癌预后有关。     

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

Background and Aims: 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. Methods: 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. Results: 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). Conclusion: 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.     

幽门螺杆菌相关胃疾病组织中P53、iNOS的表达

目的通过检测慢性浅表性胃炎、慢性萎缩性胃炎、肠上皮化生、不典型增生、胃癌组织幽门螺杆菌（Hp）和P53、一氧化氮合成酶（iNOS），探讨Hp感染与P53、iNOS表达的关系，以及Hp感染导致胃癌的可能分子机制。方法应用快速尿素酶试验和组织切片革兰氏染色和血清HpCagA抗体检测Hp，用免疫组化SP法检测上述组织的P53、iNOS。结果慢性浅表性胃炎、慢性萎缩性胃炎、肠上皮化生、不典型增生、胃癌组织中Hp检出率分别为45．9％、68．4％、71．4％、75．O％、54．8％，病变各组中P53和iNOS表达阳性率与浅表性胃炎组比较均有显著性差异。除浅表性胃炎组、萎缩性胃炎Hp阳性组的P53表达阳性率外，各病变Hp阳性组的P53和iNOS表达阳性率与各组的Hp感染阳性率呈正相关，各病变组中Hp（＋）组的P53和iNOS表达阳性率显著高于Hp（-）组，均有显著性差异。结论Hp与P53和iNOS阳性表达有一定的相关性。     

Roles of Helicobacter pylori infection and cyclooxygenase-2 expression in gastric carcinogenesis

AIM: Cyclooxygenase (COX)-2 is over expressed in gastrointestinal neoplasm. Helicobacter pylori (H pylori) infection is causally linked to gastric cancer. However, the expression of COX-2 in various stages of H pylori-associated gastric carcinogenesis pathway has not been elucidated. Therefore, the aim of this study was to clarify the role of H pylori induced COX-2 expression during carcinogenesis in the stomach. METHODS: Gastric biopsies from 138 subjects (30 cases of chronic superficial gastritis (CSG), 28 cases of gastric glandular atrophy (GA), 45 cases of gastric mucosal intestinal metaplasia (IM), 12 cases of moderate gastric epithelial dysplasia and 23 cases of gastric cancer) were enrolled. H pylori infection was assessed by a rapid urease test and histological examination (modified Giemsa staining). The expression of COX-1 and COX-2 in human gastric mucosa was detected by immunohistochemical staining. RESULTS: H pylori infection rate was 64.3% in GA and 69.5% in gastric cancer, which was significantly higher than that (36.7%) in CSG (P<0.05). The positive expression rates of COX-2 were 10.0%, 35.7%, 37.8%, 41.7% and 69.5% in CSG, GA, IM, dysplasia and gastric cancer, respectively. From CSG to GA, IM, dysplasia and finally to gastric cancer, expression of COX-2 showed an ascending tendency, whereas COX-1 expression did not change significantly in the gastric mucosa. The level of COX-2 expression in IM and dysplasia was significantly higher in H pylori-positive than in H pylori-negative subjects (P<0.01). CONCLUSION: COX-2 expression induced by H pylori infection is a relatively early event during carcinogenesis in the stomach.     

幽门螺杆菌感染和端粒酶活性以及c-myc、p16基因的表达在胃黏膜癌变中的相关性研究

幽门螺杆菌(H.pylori)是胃癌的主要致病因子,H.pylori、端粒酶和肿瘤相关基因的关系在胃黏膜癌变发生过程中研究很少。目的:观察H.pylori感染和端粒酶活性以及c-myc、p16基因在胃癌中的关系。方法:通过胃镜活检和外科手术获取171例胃组织标本,快速尿素酶试验和H.pylori培养确定有无H.pylori感染;酶联免疫法检测H.pylori感染患者的血清CagA-IgG水平;聚合酶链反应.酶联免疫吸附测定(PCR-ELISA)法检测端粒酶活性;免疫组化法检测c-myc、p16基因的表达。结果:胃癌(GC)组端粒酶表达率显著高于其他各组(P<0.01);慢性萎缩性胃炎(CAG)伴中、重度肠化(IM)组端粒酶和c-myc表达率显著高于CAG伴轻度IM组(P<0.05);而慢性浅表性胃炎(CSG)和CAG伴轻度IM组p16表达率显著高于CAG伴中、重度IM、异型增生(Dys)和GC组(P<0.05)。在CAG伴轻、中、重度IM组中,H.pylori阳性组端粒酶活性比阴性组高:无论有无H.pylori感染,胃癌组端粒酶活性都非常高。在CAG伴中、重度IM、Dys和GC组中,H.pylori阳性亚组c-myc表达显著高于阴性亚组(P<0.01),而在ECAG伴中、重度IM和Dys组中,H.pylori阳性亚组p16基因表达显著低于阴性亚组(P<0.01)。结论:H pylori感染很可能主要通过c-myc基因的激活和p16基因的失活以及其他基因的变化来诱导CAG伴中、重度     

Expression of trefoil factors 1 and 2 in precancerous condition and gastric cancer

AIM: To study the expression of trefoil factor 1 (TFF1) and TFF2 in precancerous condition and gastric cancer and to explore the relationship between TFFs and tumorigenesis, precancerous condition and gastric cancer. METHODS: The expression of TFF1 and TFF2 was immunohistochemically analyzed in paraffin-embedded samples from 140 patients including 35 cases of chronic superficial gastritis (CSG), 35 cases of gastric ulcer (GU), 35 cases of chronic atrophic gastritis (CAG) and 35 cases of gastric cancer (GC). RESULTS: TFF1 and TFF2 were located in cytoplasm of gastric mucous cells. In CSG, GU, CAG and GC, the level of TFF1 expression had a decreased tendency (P<0.05). The expression of TFF2 was higher in GU than in CSG, but the difference was not significant. The expression of TFF2 also had a decreased tendency in GU, CAG, and GC (P<0.05). CONCLUSION: The reduced expression of TFF1 and TFF2 in precancerous conditions and gastric cancer may be associated with the proliferation and malignant transformation of gastric mucosa. More investigations are needed to explore the mechanism of TFFs and the relationship between TFFs and gastric cancer.     

AgNOR and rasp21 expression in gastric mucosal lesions caused by Helicobacter pylori infection

AIM: To investigate AgNOR and rasp21 expression levels in gastric mucosal lesions caused by Helicobacter pylori (Hp) infection in order to gain insight into the related biological processes (i.e. tumor-like behavior) and possible underlying mechanism supporting Hp pathogenesis.METHODS: Hp infection was diagnosed in using the standard Campylobacter-like organism test along with Wathin-Starry staining. The expression of AgNOR was detected by the silver colloid staining technique. The expression of rasp21 was detected by monoclonal antibody and immunohistochemical staining using the ABC method. The study included a total of 278 patients with endoscopically- and pathologically-confirmed gastric mucosal lesions, representing chronic superficial gastritis (CSG), chronic atrophic gastritis (CAG), intestinal metaplasia, dysplasia, and gastric cancer. Among these, 146 of the patients were Hp-positive and 132 were Hp-negative.RESULTS: The Hp-positive group of patients showed significantly greater AgNOR in the gastric mucosal lesions than the Hp-negative group, with the exception of the CSG sub-group (P < 0.05 or P < 0.01). The positive rate of rasp21 expression in gastric mucosal lesions in the Hp-positive group was also significantly higher than that in the Hp-negative group, with the exception of the CSG and CAG sub-groups (P < 0.05).CONCLUSION: Hp-positive gastric mucosal lesions show biological behaviour of tumors. Hp may act as a promoter to activate the ras gene and to stimulate cell over-proliferation.     

幽门螺杆菌相关性胃病的细胞增殖和凋亡

目的 观察幽门螺杆菌（Hp)及其CagA基因对细胞增殖和凋亡的影响,进而探讨Hp增加胃癌发生危险性的机制。方法 研究对象为慢性浅表性胃炎（CSG）、慢性萎缩性胃炎（CAG）、慢性萎缩性胃炎伴肠上皮化生（CAGIM）、不典型增生（DYS）、胃癌（GC）患者127例及正常对照组（NS）14例。应用ki-67免疫组化技术评价幽门窦上皮细胞增生,用切口末端标记法（TUNEL）检测胃上皮细胞凋亡,应用聚合酶链反应（PCR）技术检测Hp的CagA基因。结果 Hp阳性患者的增殖指数（LI）和凋亡指数（AI）显著高于Hp阴性者或正常对照（P＜0．05和P＜0．01）。CSGHp阳性的LI和AI明显高于Hp阴性者（P＜0．01）,而其余四种胃病Hp阳性患者（P＜0．05）。Hp阳性或阴性CSG、NS组的AI与LI呈正相关,GC患者的AI与LI呈负相关。LI和AI与胃粘膜炎症程度无明显关系。结论 Hp诱导胃粘膜上皮细胞过度增殖和凋亡主要发生在Hp感染的早期,CagA^ Hp与CagA^－Hp促增殖和凋亡作用的能力明显不同,Hp感染通过引起增殖和凋亡比例的失调,最终促进肿瘤发生。     

三叶因子Ⅰ和Ⅱ在胃癌和癌前状态中的表达

目的　探讨三叶因子Ⅰ (trefoilfactor1,TFF1)和Ⅱ (TFF2 )与癌前状态及胃癌发生及发展的关系。方法　对 14 0例经病理证实的不同胃黏膜病变 ,采用免疫组化方法进行TFF1、TFF2蛋白的定位和半定量检测。结果　在慢性浅表性胃炎、胃溃疡、慢性萎缩性胃炎和胃癌 4种病变中 ,TFF1表达呈逐渐减弱趋势 (P <0 0 5)。TFF2在上述 4种病变中的表达差异亦有显著性 (P <0 0 5) ,其中在胃溃疡、慢性萎缩性胃炎和胃癌组织中 ,TFF2表达逐渐降低 (P <0 0 5)。结论　TFF1和TFF2蛋白在癌前状态和胃癌的表达降低 ,TFF1和TFF2的作用机制以及临床应用前景有待于进一步研究     

Helicobacter pylori infection and expression of the angiogenic factor platelet-derived endothelial cell growth factor by pre-neoplastic gastric mucosal lesions and gastric carcinoma

BACKGROUND: Expression of the angiogenic factor platelet-derived endothelial cell growth factor is induced in some gastric carcinomas. Whether angiogenesis is induced early in the development of gastric pre-neoplastic lesions and whether Helicobacter pylori infection affects platelet-derived endothelial cell growth factor expression is not known. AIM: To assess whether chronic gastritis, intestinal metaplasia, gastric dysplasia and gastric carcinomas express platelet-derived endothelial cell growth factor and whether Helicobacter pylori infection might affect the expression of platelet-derived endothelial cell growth factor in these lesions. PATIENTS AND METHODS: Patients with gastric carcinomas, atrophic gastritis with associated intestinal metaplasia, dysplasia and controls without infection or carcinoma were studied. RESULTS: Platelet-derived endothelial cell growth factor was detected by immunohistochemistry in 9 out 19 gastric carcinomas (45%). Only focal immunostaining was detected in intestinal metaplasia adjacent to dysplasia and in dysplastic cells. Of the tumours, 90% contained platelet-derived endothelial cell growth factor-positive interstitial cells. A significant correlation was found between active Helicobacter pylori infection and a larger number of platelet-derived endothelial cell growth factor-positive interstitial cells in areas of intestinal metaplasia (p<0.05). CCONCLUSION:Helicobacter pylori infection does not influence the expression of platelet-derived endothelial cell growth factor, once gastric cancer has developed. However, Helicobacter pylori infection may increase the extension of expression of platelet-derived endothelial cell growth factor by infiltrating interstitial cells in premalignant lesions, such as intestinal metaplasia, which may help create a favourable environment for tumour development. This may possibly be due to non-specific increase in recruitment of inflammatory cells caused by Helicobacter pylori infection. Further studies, with a larger number of samples, are now needed in order to confirm this finding.     

胃癌幽门螺杆菌感染中c-met基因表达与增殖的关系及其预后

目的 研究c-met基因蛋白及增殖细胞核抗原（PCNA）在幽门螺杆菌（Hp)感染的胃黏膜病变演进中的表达及关系，探讨Hp感染对胃癌预后的意义。方法 采用免疫组织化学法检测145例经病理证实不同胃黏膜病变的c-met和PCNA基因表达，Warthin-Starry法检测Hp感染。结果 在浅表性胃炎（CSG）、萎缩肠化性胃炎、异型增生（DYS）、早期胃癌和进展期胃癌中，c-met和PCNA2种基因在萎缩肠化性胃炎、DYS、胃癌均显著高于CSG（P＜0．05）。对胃黏膜增殖程度与c-met和PCNA阳性表达强度的密切关系分析，表明两者有显著关联（P＜0．01）。c-met和PCNA阳性表达与胃癌组织类型、浆膜浸润和淋巴结转移密切相关，而且Borrmann Ⅳ明显高于早期胃癌（P＜0．05）。c-met－LI和PCNA－LI在胃癌中等级相关表达有极显著的相关性（P＜0．001）。c-met阳性表达与肠型胃癌Hp感染有关。萎缩肠化性胃炎、DYS和胃癌组c-met阳性表达中Hp感染者明显高于阴性者。Hp阳性者5年生存期显著短于Hp阴性者。结论 c-met和PCNA基因表达与胃黏膜增殖和恶化有关，c-met基因可能成为评估胃癌恶化和预后的1项新的重要指标。Hp感染和c-met表达与胃黏膜增殖和恶化有关，Hp感染与胃癌预后有关。     

Effect of Helicobacter pylori infection and its eradication on cell proliferation, DNA status, and oncogene expression in patients with chronic gastritis.

BACKGROUND: Helicobacter pylori, the main cause of chronic gastritis, is a class I gastric carcinogen. Chronic gastritis progresses to cancer through atrophy, metaplasia, and dysplasia. Precancerous phenotypic expression is generally associated with acquired genomic instability. AIM: To evaluate the effect of H pylori infection and its eradication on gastric histology, cell proliferation, DNA status, and oncogene expression. METHODS/SUBJECTS: Morphometric and immunohistochemical techniques were used to examine gastric mucosal biopsy specimens from eight controls, 10 patients with H pylori negative chronic gastritis, 53 with H pylori positive chronic gastritis, and 11 with gastric cancer. RESULTS: All patients with chronic gastritis were in a hyperproliferative state related to mucosal inflammation, regardless of H pylori infection. Atrophy was present in three of 10 patients with H pylori negative chronic gastritis and in 26 of 53 with H pylori positive chronic gastritis, associated in 18 with intestinal metaplasia. DNA content was abnormal in only 11 patients with atrophy and H pylori infection; eight of these also had c-Myc expression, associated in six cases with p53 expression. Fifty three patients with H pylori positive chronic gastritis were monitored for 12 months after antibiotic treatment: three dropped out; infection was eradicated in 45, in whom cell proliferation decreased in parallel with the reduction in gastritis activity; atrophy previously detected in 21/45 disappeared in five, regressed from moderate to mild in nine, and remained unchanged in seven; complete metaplasia disappeared in 4/14, and markers of genomic instability disappeared where previously present. In the five patients in whom H pylori persisted, atrophy, metaplasia, dysplasia, and markers of genomic instability remained unchanged. CONCLUSIONS: Chronic H pylori infection seems to be responsible for genomic instability in a subset of cases of H pylori positive chronic atrophic gastritis; eradication of H pylori infection can reverse inflammation and the related atrophy, metaplasia, and genomic instability.     

Hp相关性胃疾病与胃肠化生、不典型增生的关系

目的探讨Hp感染与肠化生、不典型增生等胃癌前期病变的关系.方法693例胃病患者,分慢性浅表性胃炎(CSG)、慢性萎缩性胃炎(CAG)、胃溃疡(GU)及十二指球部溃疡(DU)等四组,胃镜下观察粘膜病变、溃疡部位及性质,胃镜下取材,常规HE染色后观察组织学改变、Giemsa染色后观察Hp感染程度,统计分析Hp感染与肠化生、不典型增生等的关系.结果四组胃疾病中,Hp感染程度与肠化尘程度差异显著(P＜0.01),DU组的Hp感染率高于其它组(P＜0.01),CAG组的胃肠化生率最高(P＜0.05);Hp阳性标本中,CAG组的胃肠化及不典型增生最高(P＜0.01)Hp阴性标本中,CAG组的胃肠本的胃肠化和不典型增生发生率与Hp阴性标本的发生率有显著差异(P＜0.05).结论Hp与CAG并存时,癌前病变发生率最高,其次为GU;建议在临床上,抗Hp治疗和对CAG、GU的治疗同时进行,并内镜随访.     

Effect of non-steroidal anti-inflammatory drugs on gastric and duodenal prostaglandin concentrations in patients with Helicobacter pylori infection.

BACKGROUND/AIMS: Both Helicobacter pylori and non-steroidal anti-inflammatory drugs are reported to affect gastroduodenal prostaglandin synthesis. However, their influence on gastric mucosal prostaglandins remains unclear. The aim of this study was to investigate the influence of nonsteroidal anti-inflammatory drugs on mucosal prostaglandin synthesis in patients with Helicobacter pylori infection. METHODOLOGY: We enrolled 87 Helicobacter pylori-infected patients in this study (gastric ulcer: 33, duodenal ulcer: 41, and non-ulcer dyspepsia: 13). Of them, 27 patients received non-steroidal anti-inflammatory drugs. Endoscopy was performed and biospy specimens from gastric body, antrum and duodenal bulb were assessed for Helicobacter pylori and prostaglandin concentration. RESULTS: A significantly lower mucosal prostaglandin E2 level at gastric body (142.2 +/- 28.1 ng/mg vs. 222.0 +/- 12.4 ng/mg, mean +/- SEM) and antrum (131.3 +/- 26.4 ng/mg vs. 226.0 +/- 19.0 ng/mg) was noted in Helicobacter pylori-infected gastric ulcer patients with non-steroidal anti-inflammatory drugs ingestion than in that of patients without non-steroidal anti-inflammatory drugs ingestion (p < 0.05). Using a multivariate analysis, we found that non-steroidal anti-inflammatory drug was an independent variable affecting gastric and duodenal mucosal prostaglandin E2 synthesis in patients with Helicobacter pylori-infected gastric ulcer. CONCLUSIONS: Non-steroidal anti-inflammatory drugs decrease gastroduodenal mucosal prostaglandin E2 synthesis in gastric ulcer patients with Helicobacter pylori infection.     

Dynamic expression of pepsinogen C in gastric cancer, precancerous lesions and Helicobacter pylori associated gastric diseases

AIM: To investigate the relationship between the expression of pepsinogen C (PGC) and gastric cancer, precancerous diseases, and Helicobacter pylori (H pylori) infection. METHODS: The expression of PGC was determined by immunohistochemistry method in 430 cases of gastric mucosa. H3 Pylori infection was determined by HE staining, PCR and ELISA in 318 specimens. RESULTS: The positive rate of PGC expression in 54 cases of normal gastric mucosa was 100%. The positive rates of PGC expression in superficial gastritis or gastric ulcer or erosion, atrophic gastritis or gastric dysplasia and gastric cancer decreased significantly in sequence (P<0.05; 100%/89.2% vs 14.3%/15.2% vs 2.4%). The over-expression rate of PGC in group of superficial gastritis with H pyloriinfection was higher than that in group without H pylori infection (P<0.05; x2= 0.032 28/33 vs 15/25). The positive rate of PGC expression in group of atrophic gastritis with H pylori infection was lower than that in group without H pylori infection (P<0.01; x2 = 0.003 4/61 vs9/30), and in dysplasia and gastric cancer. CONCLUSION: The level of PGC expression has a close relationship with the degree of malignancy of gastric mucosa and development of gastric lesions. There is a relationship between H pylori infection and expression of antigen PGC in gastric mucosa, the positive rate of PGC expression increases in early stage of gastric lesions with H pylori infection such as gastric inflammation and decreases during the late stage such as precancerous diseases and gastric cancer. PGC-negative cases with H py/ori-positive gastric lesions should be given special attention.     

胃癌中幽门螺杆菌感染与胃粘膜增殖及凋亡研究

目的研究幽门螺杆菌(Hp)感染的胃癌(GC)发展中增殖细胞核抗原(PCNA)表达及细胞凋亡的关系和对胃癌预后意义。方法145例经病理证实,不同胃黏膜病变采用免疫组化检测PCNA基因表达及Warthinstarry法检测Hp感染。采用原位末端标记法(TUNEL)检测细胞凋亡。结果在浅表性胃炎(CSG)、萎缩肠化生胃炎(CAG+IM)、异型增生(DYS)、早期GC和进展期GC中,PCNA基因表达率分别为24.53%,46.28%,60.54%,57.67%和71.42%,CAG+IM、DYS、GC均显著高于CSG(P<0.05)。凋亡指数(AI)分别为(4.55±2.33)%、(6.43±5.60)%、(6.45±5.12)%、(6.55±4.80)%、(8.84±5.63)%,进展期GC显著高于CSG(P<0.05)。胃黏膜凋亡指数与PCNA表达强度有密切相关(P<0.05)。PCNA阳性表达与胃癌组织类型、浆膜浸润和淋巴结转移密切相关,而且BorrmannIV明显高于早期胃癌和BorrmannI,II(P<0.05)。PCNA阳性表达与肠型胃癌Hp感染有关。CAG+IM,DYS和GC组PCNA阳性表达中Hp感染者明显高于阴性者。Hp阳性者5年生存期显著短于Hp阴性者。结论Hp感染和PCNA表达与胃黏膜增殖和恶化有关,且与凋亡有相关性。Hp感染与胃癌预后有关。     

TFF2在幽门螺杆菌感染胃体部黏膜中的表达

目的:探讨三叶因子2(TFF2)在幽门螺杆菌(H pylori)感染胃体腺黏膜中表达的意义.方法:选择有H pylori感染的胃手术切除标本29例(92个蜡块),其中胃及十二指肠溃疡5例,胃癌24例,用免疫组织化学方法检测TFF2的分布和表达.结果:在H pylori感染胃黏膜中,TFF2主要在胃体腺的颈黏液细胞和假幽门腺化生细胞中表达;在正常黏膜中TFF2主要分布在胃固有腺的上1/3-2/3;在轻度萎缩黏膜中,腺底部仅见少量阳性细胞,随着萎缩程度的加重,在腺底部出现的阳性细胞增多;在轻、中度萎缩黏膜中其强阳性率分别为18.0%和42.9%,而在重度萎缩中达90.5%.在轻、中度和重度萎缩之间有显著性差异(P<0.01).结论:H pylori感染增加在腺底部的TFF2表达,并与黏膜的萎缩程度有关.     

Plasma and gastric tissue selenium levels in patients with Helicobacter pylori infection

GOALS: We investigated plasma and gastric mucosal selenium levels in patients with Helicobacter pylori (HP)-associated histopathologic findings in their gastric antral mucosa. STUDY: Before and after a successful HP eradication therapy, we quantitated the plasma and antral selenium levels in patients with HP-associated chronic antral gastritis using atomic absorption flame emission spectrometry. The same measurements were done in patients with dyspeptic complaints who had normal antral histology and negative urease test. RESULTS: Thirty-four patients were studied, of whom 24 had HP-associated chronic antral gastritis confirmed by histology and positive urease test; the control group included 10 healthy patients. There was no difference between the groups with regard to age, gender, and number of smokers. All patients with HP infection were diagnosed with diffuse antral gastritis. Histopathology showed that 11 (49%) had some degree of atrophy. Of the 11 patients, 7 were classified as having chronic atrophic gastritis (CAG) without intestinal metaplasia (IM), 4 had IM, and none had dysplasia. The plasma concentrations of selenium were found to be very similar in controls and HP-infected subjects (68.0 +/- 25.97 microg/L and 71 +/- 32.9 microg/L, respectively; p > 0.05). The antral biopsy samples of the patients with HP-associated gastritis contained significantly higher levels of tissue selenium than the controls (20.17 +/- 19.74 microg/g and 2.83 +/- 1.42 microg/g, respectively; p < 0.05). Also, it was shown that antral tissue selenium levels decrease after successful HP eradication therapy (20.17 +/- 19.4 microg/g and 7.4 +/- 4.56 microg/g, respectively; t < 0.05). The patients with HP gastritis were assigned to mild, moderate, and severe gastritis groups, according to the histopathologic degree of inflammation present. The antral gastric selenium levels were significantly higher in patients with moderate and severe HP gastritis (21.13 +/- 22.5 microg/g and 22.81 +/- 17.35 microg/g, respectively) than in patients with mild gastric inflammation (9.53 +/- 10.3 microg/g; p < 0.05). The selenium concentrations in the biopsies of patients with CAG were significantly lower than in those with HP gastritis who did not have CAG (9.45 +/- 6.44 microg/g vs. 19.13 +/- 22.48 microg/g, respectively; p < 0.05). CONCLUSIONS: Selenium accumulates in gastric tissue when it is needed, as is the case in HP-related antral inflammation. This reactive increase in gastric mucosal selenium seems to disappear in the presence of precancerous gastric lesions in the setting of HP-associated gastritis.     

胃黏膜病变演化过程中抗氧化蛋白Peroxiredoxin6的表达及其与幽门螺杆菌感染的关系

目的探讨胃黏膜病变演化过程中抗氧化蛋白Peroxiredoxin 6(Prx6)表达水平变化及其与幽门螺杆菌(H.pylori)感染的关系。方法根据组织形态学将104例临床内镜检查活检标本分为慢性浅表性胃炎(33例)、慢性萎缩性胃炎(25例)、肠上皮化生(32例)及异型增生(14例)4组。用免疫组织化学方法检测组织标本中Prx6的表达水平。用快速尿素酶试验及Warthin-Starry银染检测H.pylori感染。结果 Prx6在慢性浅表性胃炎、慢性萎缩性胃炎、肠上皮化生、异型增生组的阳性表达率分别为39.4%(13/33)、80.0%(20/25)、93.8%(30/32)、92.9%(13/14),过表达率分别为15.2%(5/33)、44.0%(11/25)、81.3%(26/32)、85.7%(12/14)。慢性浅表性胃炎、慢性萎缩性胃炎组H.pylori阳性者Prx6阳性表达率显著高于H.pylori阴性者(P<0.05),肠上皮化生组Prx6的表达在H.pylori阳性者和阴性者无显著差异(P>0.05)。结论在胃黏膜病变演化过程中,Prx6的表达随着胃黏膜病变的进展而增加,H.pylori在胃黏膜病变演化的早期阶段促进了Prx6的表达。