胃粘膜癌变过程中幽门螺杆菌感染与端粒酶活性的表达

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目的分析不同病变胃粘膜端粒酶活性表达的差异,及其与Hp 感染的关系,并探讨端粒酶活性表达、Hp 感染和胃粘膜癌变的关系.方法应用 TRAP 测定172例内镜活检标本和45例胃癌手术标本的端粒酶活性,其中内镜活检标本正常胃粘膜10例、慢性浅表性胃炎46例、胃溃疡30例、慢性萎缩性胃炎68例、胃癌18例,手术标本高分化型胃癌8例、低分化型胃癌37例.同时用 EIA 检测 Hp 感染患者血清中 Hp-CagA-IgG,并分析端粒酶活性的表达和 Hp-CagA-IgG 水平的关系.结果在172例内镜活检标本中,正常胃粘膜、慢性浅表性胃炎、慢性萎缩性胃炎伴0度、1度、2度肠化和胃癌组织的端粒酶阳性率分别为0%,0%,0%,25%,38%,89%.45例手术切除的胃癌组织和相应的非癌胃组织也展现了相似的结果.Hp检出情况,正常胃粘膜、浅表性胃炎、慢性萎缩性胃炎伴0度、1度、2度肠化 Hp 阳性率分别为0%,52%,60%,70%,75%.45例手术切除胃癌的非癌胃组织伴0度、1度、2度肠化的 Hp 感染强度分别为10.8±9.6,41.3±31.1,86.4±47.8个/50腺体.慢性浅表性胃炎患者的 Hp-CagA-IgG 抗体显著低于胃癌患者的 Hp-CagA-IgG 抗体水平(P<0.01),22例 Hp 阳性的胃癌患者感染的 Hp 全部为 CagA~+株,其非癌胃粘膜有12例展现了端粒酶活性(55%);相反 Hp 阳性的22例慢性浅表性胃炎患者感染的 Hp 只有8例为 CagA~+株(36%),其胃粘膜均未展现端粒酶活性.结论正常胃粘膜和浅表性胃炎不表达端粒酶活性.萎缩性胃炎随肠化进展端粒酶活性表达增加,胃癌组织中端粒酶活性表达最高,阳性率达88%以上.在胃癌患者的非癌胃粘膜中端粒酶活性的表达与肠化程度、Hp 感染强度呈平行关系,且感染的Hp 多为 CagA~+株;而慢性浅表性胃炎感染的 Hp 多为 CagA株.端粒酶活性检测可以作为胃粘膜癌变的一个早期预测指标,CagA~+的 Hp 感染可能是端粒酶重新激活的一个启动信号. Objective To analyze the difference of telomerase activity in gastric mucosa with different pathological changes and its relationship with Hp infection and explore the relationship between telomerase activity, Hp infection and gastric mucosal carcinogenesis.Methods 172 cases of endoscopic biopsy specimens Among the 45 gastric cancer specimens, 10 had normal gastric mucosa, 46 with chronic superficial gastritis, 30 with gastric ulcer, 68 with chronic atrophic gastritis, 18 with gastric cancer, 8 cases of gastric cancer and 37 cases of poorly differentiated gastric cancer.At the same time, Hp-CagA-IgG was detected by EIA in patients with Hp infection, and the relationship between the expression of Hp-CagA-IgG and the expression of Hp-CagA-IgG was analyzed.Results In 172 cases In the biopsy specimens, the positive rates of telomerase in normal gastric mucosa, chronic superficial gastritis and chronic atrophic gastritis with 0 degrees, 1 degree and 2 degrees of intestinal metaplasia and gastric cancer were 0%, 0%, 0% 25%, 38%, 89% .45 cases of resected gastric cancer tissue and the corresponding non-cancerous gastric tissue also showed similar results.Hp detection, normal gastric mucosa, superficial gastritis, chronic atrophic gastritis with 0 Degree, 1 degree, 2 degree of intestinal Hp positive rate were 0%, 52%, 60%, 70%, 75% .45 cases The intensity of Hp infection in non-cancerous gastric tissues with 0, 1 and 2 degrees of intestinal metaplasia was 10.8 ± 9.6, 41.3 ± 31.1 and 86.4 ± 47.8 / 50, respectively.Hp in patients with chronic superficial gastritis CagA-IgG antibody was significantly lower than that of Hp-CagA-IgG antibody in patients with gastric cancer (P <0.01). All Hp-positive gastric cancer patients were infected with CagA + strains and Hp-CagA- Telomerase activity (55%). In contrast, 22 Hp-positive cases of chronic superficial gastritis had only 8 cases of CagA + strains (36%), and no telomerase activity was found in gastric mucosa. In normal gastric mucosa and superficial gastritis, telomerase activity was not expressed.Western blotting showed that the expression of telomerase activity was increased with the development of intestinal metaplasia, and the telomerase activity was the highest in gastric cancer tissues with a positive rate of over 88% The expression of telomerase activity in non-gastric mucosa was in parallel with the degree of intestinal metaplasia and Hp infection, and most of the infected Hp were CagA ~ + strains, while Hp in chronic superficial gastritis was mostly CagA. Enzyme activity detection can be used as an early predictive indicator of gastric cancer, Hp infection of CagA ~ + may be telomerase reactivation A start signal.
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