摘要
目的:探讨不同表型的幽门螺杆菌(Hp)对胃黏膜k i-67表达的影响。方法:对137例经胃镜及组织学检查确诊的Hp(+)慢性胃炎(CG)、消化性溃疡及胃癌患者和34例Hp(-)患者,用W estern b lot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(C I)、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k i-67的表达。结果:①Hp相对分子质量为128 000CagA、116 000 CagA、95 000VacA、91 000VacA、30 000UreA的表达在轻度C I组的比例低于中、重度C I组(P<0.05),95 000VacA、91 000 VacA和30 000UreA表达在无PA组的比例低于有PA组(P<0.05)。②k i-67标记指数(LI)在慢性胃炎Hp(+)组高于Hp(-)组(P=0.041);在中、重度DH组高于轻度组(P=0.014);在Hp(+)CG中重度C I组高于轻度组(P=0.039),而在Hp(-)CG组则无此关系(P>0.05)。Hp(+)CG中,128 000 CagA、95 000VacA、30 000UreA表达组k i-67LI高于相应不表达组(P<0.05);Hp(+)胃癌者中,128 000 CagA表达组k i-67LI高于相应不表达组(P=0.02)。结论:Hp多种毒力因子对加重胃黏膜C I程度、PA的发生和发展起促进作用,Hp感染及DH增加均促进慢性胃炎胃黏膜上皮细胞增殖,但可能对胃黏膜良恶性病变的促细胞增殖作用有差异,更多毒力因子对慢性胃炎而不是胃癌的细胞增殖起作用。
Objective ： To explore the effects of different Helicobacter pylori （Hp） phenotype on expression of ki-67 in gastric mucosa. Methods： 137 patients （with Hp infection） with chronic gastritis （ CG）, peptic ulcer or gastric cancer and 34 patients without Hp infection were observed. All patients with gastroduodenal diseases were diagnosed by endoscopy and histology. Western blotting was used to detect phenotypes of Hp Cytotoxin-associated protein （ CagA）, vacuolating cytotoxin （ VacA）, Urease and their sub-phenotypes. In Hp associated gastritis, histological grade of chronic inflammation （CI）, polymorphonuclear neutrophil activity （PA） and density of Hp （DH） were scored according to the Updated Sydney System. Immunohistochemistry was used to exam the expression of ki-67. Results：①Expression rates of Hp128 000 CagA, 116 000 CagA, 95 000 VacA, 91 000 VacA and 30 000 UreA in the group of mild grade of CI were lower than those in the moderate-marked group （ P 〈 0.05, respectively） ; Hp infection rate and expression rates of 95 000 VacA, 91 000 VacA and 30000 UreA in the group of mild grade of PA were lower than those in the moderate-marked group （P 〈0.05 ,respectively）. ②ki-67LI in Hp（ ＋ ） CG group were higher than that of Hp（ - ） CG group （P =0. 041 ）. In Hp（ ＋ ） CG, ki-67LI in the group of moderate-marked grade of DH was higher than that in the mild grade of CI group （ P = 0.014）. In Hp（ ＋ ） CG, ki-67LI in the group of moderate-marked grade of CI was higher than that in the mild grade of CI group （P = 0.039）, while no significances were found in Hp（ - ） CG group （P 〉 0.05, respectively）. ③In Hp（ ＋ ） CG, ki-67LI in the group with expression of 128 000 CagA, 95000VacA or 30 000 UreA were higher than that in groups without their expression. In Hp （ ＋ ） gastric cancer, ki-67LI in the group with expression of 128000 CagA was higher than that in the group without its expression （ P = 0. 02 ）. Conclusion ： Many virulent factors of Hp may cause increased grade of CI and play an important role in the occurrence and development of PA. Hp infection and density of Hp seem to cause increased epithelial cell proliferation in gastric mucosa with chronic gastritis. But they may exert different influences on malignant and benign gastric mucosa, and more virulent factors probably increase epithelial cell proliferation in gastric mucosa with chronic gastritis rather than gastric cancer.
出处
《医学研究生学报》
CAS
2005年第9期808-811,共4页
Journal of Medical Postgraduates
关键词
幽门螺杆菌
表型
慢性胃炎
胃癌
KI-67
Helicobacter pylori
Phenotype
Chronic gastritis
Gastric cancer
ki-67
