胃癌形成中Hp感染与其细胞凋亡和增殖的关系

目的 研究胃癌（gastriccancer，GC）形成中胃幽门螺杆菌（Helicobacterpylori，Hp）感染规律与其细胞凋亡、增殖的关系，探讨Hp在GC形成中的可能作用机制。方法 采用免疫组织化学染色法（SABC法）和末端脱氧核苷酸转移酶（TDT）介导的dUTP缺口标记法（TUNEL）检测15例正常胃黏膜（normalgastricmucosa，NGM）、30例胃黏膜肠上皮化生（intesunal metaplasia，IM）、30例异型增生（Dysplasia，Dys）和40例GC组织中增殖细胞核抗原（proliferating cellnuclear antigen，PCNA）阳性袁达和细胞凋亡情况，用Warthin—Starry染色方法、快速尿素酶试纸检测组织中Hp感染率。结果在NGM→IM→Dy→Gc的形成过程中，Hp感染随着GC形成中病变恶性程度的加重而明显上升，Hp感染率在IM（66．7％）、Dys（83．3％）、GC（60．0％）中显著高于NGM（20．0％）。IM组Hp阳性者AI、PI均明显高于Hp阴性者（p〈0．01），其余3组差异无显著性（P〉0．05）。结论 Hp感染可能参与胃癌癌前病变乃至胃癌的发生，Hp感染促进胃黏膜细胞凋亡、增殖作用主要发生在胃癌癌前病变早期阶段。

Hp infection in gastric carcinogenesis and their correlation with cell apoptosis and cell proliferation

[Objectives] To study infection of Helicobacter pylori (Hp) in the gastric carcinogensis and their relation with cell apoptosis, proliferation, and to explore their possible roles in the gastric carcinogenic mechanism. [Methods] Gastric tissue specimens were obtained from 15 cases with normal gastric mucosa (NGM), 30 with intestinal metaplasia (IM), 30 with dysplasia (Dys) and 40 with gastric cancer (GC). Proliferating cell nuclear antigen (PCNA) was detected by immunohistochemistry ( with SABC method ), and cell apoptosis was measured by TUNEL. Infection of Hp was determined through Warthin-Starry staining and rapid urease test (RUT). [Results] Infection rate of Hp in GC (60.0%), IM (66.7%) and Dys (83.3%) was apparently higher than that in NGM (20.0%). In IM AI and PI with Hp infection were higher than that without Hp infection (P <0.01), but there were not differences between the other three groups. [Conclusion] Hp infection may involve in gastric carcinogenesis. And at the early stages of gastric carcinogenesis Hp infection can stimulate cell proliferation and cell apoptosis.