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为探讨幽门螺杆菌（Ｈｐ）在胃癌发生过程中的作用机制，采用了免疫组织化学和Ｎｏｒｔｈｅｒｎ－ｂｌｏｔ方法，对３５例慢性胃炎和２０例胃腺癌患者进行了对比观察，其中２４／３５例慢性胃炎检出Ｈｐ，另１１／２０例胃腺癌为Ｈｐ阳性。Ｈｐ相关慢性胃炎者增殖细胞核抗原（ＰＣＮＡ）标计指数（ＬＩ）为２０．６±４．７，高于Ｈｐ阴性慢性胃炎ＬＩ（１１．３±５．２）（Ｐ＜０．０５）；Ｈｐ阳性胃腺癌组织ＨＳＰ７０表达水平低于Ｈｐ阴性胃腺癌者，并低于Ｈｐ阳性的慢性胃炎者。结果提示，Ｈｐ感染的存在，可能具有促使慢性胃炎者胃粘膜增生，降低胃腺癌ＨＳＰ７０表达的作用
In order to investigate the mechanism of Helicobacter pylori (Hp) in gastric carcinogenesis, immunohistochemistry and Northern-blot methods were used to compare 35 cases of chronic gastritis and 20 cases of gastric adenocarcinoma, of which 24/35 cases were chronic. Hp was detected in gastritis, and another 11/20 cases of gastric adenocarcinoma were Hp positive. The proliferating cell nuclear antigen (PCNA) labeling index (LI) of Hp-associated chronic gastritis was 20.6±4.7, which was higher than that of Hp-negative chronic gastritis LI (11.3±5.2) (P<0.05). The expression of HSP70 in Hp-positive gastric adenocarcinoma was lower than that in Hp-negative gastric adenocarcinoma, and lower in Hp-positive chronic gastritis. The results suggest that the presence of Hp infection may have the effect of promoting gastric mucosal hyperplasia and reducing the expression of HSP70 in gastric adenocarcinoma in patients with chronic gastritis.