Hp感染与不同类型上消化道疾病中Cyclin D1表达相关性研究

目的研究不同类型上消化道疾病中幽门螺杆菌(Hp)感染率、东亚型Cag A阳性Hp感染率及与Cyclin D1表达的相关性,探索Hp致胃癌及其癌前病变的机制。方法采用免疫组化链霉菌抗生素蛋白-过氧化物酶连接法(SP)法分别检测慢性浅表性胃炎(CSG)、慢性萎缩性胃炎(CAG)、十二指肠球部溃疡(DU)、胃溃疡(GU)和胃癌(GCA)患者胃体、胃窦组织中Cyclin D1的表达变化,及Hp、东亚型Cag A阳性Hp感染率。结果 CSG、CAG、GCA患者胃体、胃窦组织中Cyclin D1蛋白表达阳性率逐渐升高(P0.05)。Hp阳性者胃体、胃窦组织中Cyclin D1表达明显高于Hp阴性者(P0.05)。东亚型Cag A阳性者Cyclin D1表达明显高于东亚型Cag A阴性者(P0.05)。结论胃黏膜癌变过程中的Cyclin D1阳性表达呈递增趋势,Hp感染特别是东亚型Cag A阳性Hp感染导致Cyclin D1过量表达,使细胞周期调节紊乱,有助于肿瘤的发生。

The relationship between Helicobacter pylori infection and expression of Cyclin D1 in different upper gastrointestinal disease

Objective To investigate the relationship among Helicobacter pylori infection,East-Asian CagA Helicobacter pylori infection and expression of Cyclin D1 in different upper gastrointestinal disease. Methods The Helicobacter pylori infection, East-Asian CagA Helicobacter pylori infection and expressions of Cyclin D1 in tissues from antrum and corpus in cases of chronic superficial gastritis （CSG）, chronic atrophic gastritis （CAG）, duodenal ulcer （DU）, gastric ulcer （GU） and gastric cancer （GC） were detected by immunohistochemical streptavidin-perosidase （SP） method. Results The positive expression rates of Cyclin D1 proteinin tissues from antrum and corpus increased with the progressing from CSG→CAG→ GCA （P〈0.05）. The expression levels of Cychn D1 protein in tissues from antrum and corpus of Helicobacter pylori positive cases were significantly higher than that of Helicobacter pylorinegative cases（P〈0.05）. The expressions of Cyclin D1 protein in tissues from antrum and corpus of East-Asian CagA Helicobacter pylori positive cases were significantly higher than that of East-Asian CagA Helicobacter pylori negative cases （P〈0.05）. Conclusion The expression rates of Cyclin D1 in the canceration course of the stomach mucosa are increased. Helicobacter pylori infection, especially East- Asian CagA Helicobacter pylori infection resulted in higher expiession of Cyclin D1.That resulted in the regulation disorder of cell cycle and conduced to the pathogenesis of gastric carcinoma.