幽门螺杆菌感染与不同胃粘膜病变中c-myc、Bcl-2和Bax表达的关系

背景与目的:幽门螺杆菌(Helicobacterpylori,HP)是确定的胃癌致癌因子之一,但其致癌的确切机制仍不清楚。本实验研究不同胃粘膜病变中幽门螺杆菌感染与细胞增生、凋亡的关系,探讨HP致胃癌发生的可能机制。方法:选择272例病例,包括慢性胃炎(chronicgastritis,CG)42例,肠上皮化生(intestinalmetaplasia,IM)Ⅰ～Ⅱ46例,IMⅢ25例,轻度不典型增生(dysplasiaⅠ,DysⅠ)21例,中、重度不典型增生(DysⅡ～Ⅲ)54例及胃癌(gastriccancer,GC)84例。采用Warthin-Starry细菌染色及SP免疫组化法检测HP的感染情况;HID-AB(pH2.5)-PAS粘液染色检测胃粘膜上皮及肿瘤组织中的粘液性质;SP法检测c-myc、Bcl-2和Bax的表达。采用卡方检验、Fishers精确概率法进行率的比较。结果:(1)在CG、IM、Dys、GC的胃粘膜病变标本中,c-myc、Bcl-2的表达率依次增加,而Bax的表达率则依次降低。c-myc在GC中的表达率显著高于DysⅡ～Ⅲ及IMⅢ(均P<0.01),而Bax在GC中的表达率明显低于DysⅡ～Ⅲ及IMⅢ(P<0.05或P<0.01)。(2)c-myc在IMⅢ、DysⅡ～Ⅲ病变的HP感染组中的表达率分别为62.50%、66.67%,明显高于非感染组的11.11%、27.78%(均P<0.05)。Bax在CG、IMⅠ～Ⅱ和IMⅢ病变的HP感染组中的表达率分别为87.10%、81.25%、62.50%,明显高于非感染组的54.55%

Relationship between Helicobacter pylori infection and expression of c-myc, Bcl-2, and Bax protein in different gastric mucosa lesions

BACKGROUND & OBJECTIVE: Helicobacter pylori (HP) has been believed to be a carcinogen of gastric carcinoma. However, its mechanism was yet not clearly understood. This study was designed to investigate the relationship between HP infection and gastric epithelial cell proliferation as well as apoptosis in different gastric mucosa lesions and elucidate the probable mechanism of gastric carcinogenesis relating with HP infection. METHODS: A total of 272 cases were available for the study including 42 cases of chronic gastritis (CG), 46 cases of intestinal metaplasia I or II (IM I- II), 25 cases of intestinal metaplasia III (IM III), 21 cases of mild dysplasia (Dys I), 54 cases of modest or severe dysplasia (Dys II- III), and 84 cases of gastric cancer (GC). HP infection was detected by Warthin-Starry bacterium staining method and streptavidin-peroxidase (SP) immunohistochemical method. HID-AB(pH2.5)- PAS method was used to define the quality of mucus. The expression of c-myc, Bcl-2, and Bax were detected using SP immunohistochemical method. The chi-square test and the Fisher's exact probability test were used to compare the frequencies. RESULTS: (1)The expression of c-myc and Bcl-2 increased as gastric mucosa lesions developed from CG,IM,Dys to GC,but the expression of Bax decreased. The expression of c-myc was significantly higher in GC than that in Dys II- III and IM III(all P< 0.01), but the expression of Bax was significantly lower in GC than that in Dys II- III and IM III(P< 0.05 or P< 0.01). (2)The expression of c-myc in IM III and Dys II- III with HP infection was 62.50% and 66.67%,respectively, significantly higher than that without infection(11.11%,27.78%,all P< 0.05). The expression of Bax in CG, IM I- II and IM III with HP infection were 87.10%, 81.25%, and 62.50%, respectively, significantly higher than those without infection (54.55%, 42.86%, 11.11%, all P< 0.05). Furthermore HP infection was associated with the expression of Bcl-2 in IM III, Dys II- III and GC (P< 0.05 or P< 0.01). CONCLUSION: HP infection can cause serious imbalance between cell proliferation and apoptosis in the precancerous lesions (IM III and Dys II- III), giving chances for gastric carcinogenesis.