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目的:探讨不同表型幽门螺杆菌(Hp)对Hp相关性胃炎和胃癌病变及其p53表达的影响。方法:对137例Hp(+)慢性胃炎(CG)、消化性溃疡及胃癌患者和34例Hp(-)患者用Westernblot检测Hp细胞毒素相关蛋白(CagA)、空泡毒素(VacA)、尿素酶(Urease)及其亚型。评价Hp(+)CG中慢性炎症(CI)、多形核活动性(PA)、Hp定植密度(DH)的组织学等级。用免疫组化检测p53表达,以H-score方法评价。结果:①Hp128kuCagA、116kuCagA、95kuVacA、91kuVacA、30kuUreA表达在轻度CI组的比例低于中、重度CI组(P均<0.05),95kuVacA、91kuVacA和30kuUreA表达在无PA组的比例低于有PA组(P均<0.05)。②Hp(+)组P53Hscore均高于Hp(-)CG组(P=0.002)。在Hp+CG中,中重度CI组P53Hscore均高于轻度组(P=0.025),而在Hp(-)CG组中,差异无显著性。③Hp+胃癌中,未发现任何独立表型与CG和胃癌的53Hscore有关(P>0.05)。结论:Hp多种毒力因子对胃黏膜CI程度加重、PA的发生和发展起促进作用,Hp感染及DH增加均促进p53表达无关;未见Hp任何独立表型与53表达有关,提示Hp可能通过多种毒力因素及此研究未提及的其他因素的综合作用促进p53过度表达。
Objective: To investigate the effects of different phenotypes of Helicobacter pylori (Hp) on Hp-related gastritis and gastric cancer and its p53 expression. Methods: 137 cases of Hp (+) chronic gastritis (CG), peptic ulcer and gastric cancer and 34 cases of Hp (-) were detected by Western blot with Hp cytotoxin related protein (CagA), vacuolating toxin (VacA), urease (Urease) and its subtypes. The histological grade of chronic inflammatory (CI), polymorphonuclear activity (PA), and Hp colonization density (DH) in Hp (+) CG was evaluated. The expression of p53 was detected by immunohistochemistry and evaluated by H-score method. Results: ①The expression of Hp128kuCagA, 116kuCagA, 95kuVacA, 91kuVacA, 30kuUreA in mild CI group was lower than those in moderate and severe CI group (all P <0.05). The expression of 95kuVacA, 91kuVacA and 30kuUreA in non-PA group was lower than that in PA group (P <0.05). ② P53Hscore in Hp (+) group was higher than that in Hp (-) CG group (P = 0.002). In Hp + CG, P53Hscore of moderate and severe CI group was higher than that of mild group (P = 0.025), but no significant difference in Hp (-) CG group. ③ In Hp + gastric cancer, no independent phenotype was found to be associated with 53Hscore of CG and gastric cancer (P> 0.05). CONCLUSION: Hp multi-virulence factors have a positive effect on the degree of gastric mucosal CI and the development and progression of PA. Hp infection and DH increased p53 expression. No independent phenotype of Hp was associated with 53 expression, suggesting that Hp may be The combination of multiple virulence factors and other factors not mentioned in this study promotes p53 overexpression.