论文部分内容阅读
目的：探讨幽门螺杆菌ＨＰ引起胃粘膜上皮细胞凋亡和增殖改变及ＨＰ致癌作用的可能机制。方法：采用免疫组织化学方法及脱氧核糖核酸末端转移酶介导的ｄＵＴＰ缺口末端标记（ＴＵＮＥＬ）技术，对ＨＰ阳性和ＨＰ阴性者胃粘膜上皮中增殖细胞，凋亡细胞进行原位观察和比较，同时检测 ｂｃ１－２／ｂａｘ蛋白表达状态。结果： ＨＰ阳性者胃粘膜上皮细胞增殖指数和凋亡指数显著高于ＨＰ阴性者（Ｐ＜０．０１）。ｂａｘ蛋白表达阳性率在ＨＰ阳性组较ＨＰ阴性组升高显著（ Ｐ＜ ０． ０１），而 ｂｃｌ－２蛋白表达阳性率两组差异不显著（ Ｐ＞ ０． ０５）。在 ＨＰ阳性慢性胃炎中， ｂｃｌ－２蛋白表达阳性组细胞凋亡指数显著低于阴性组（Ｐ＜０．０１）。ｂａｘ蛋白表达阳性组细胞凋亡指数显著高于阴性组（Ｐ＜０．０１）。结论：ＨＰ可诱导胃粘膜上皮细胞凋亡和过度增殖，ｂｃｌ－２蛋白低表达和ｂａｘ蛋白高表达参与此调节机制，推测认为ＨＰ在胃癌的发生过程中可能有重要意义。
Objective: To investigate the possible mechanism of Helicobacter pylori (HP) -induced apoptosis and proliferation of gastric mucosal epithelial cells and carcinogenesis of HP. Methods: The proliferating cells and apoptotic cells in gastric mucosal epithelium of HP positive and HP negative were observed and compared in situ by immunohistochemical method and DNA end-transferase-mediated dUTP nick end labeling (TUNEL) Meanwhile, the bc1-2 / bax protein expression was detected. Results: Proliferation index and apoptosis index of gastric epithelial cells in HP positive group were significantly higher than those in negative HP group (P <0.01). The positive rate of bax protein expression in HP positive group was significantly higher than that in HP negative group (P <0.01), while the positive rate of bcl-2 protein expression was not significantly different between the two groups (P> 0.05). In HP positive chronic gastritis, the apoptotic index of bcl-2 protein positive group was significantly lower than that of negative group (P <0.01). The apoptosis index of bax protein positive group was significantly higher than that of negative group (P <0.01). Conclusion: HP can induce gastric mucosal epithelial cells apoptosis and over-proliferation, low expression of bcl-2 protein and high expression of bax protein involved in this regulatory mechanism, presumably that HP in the occurrence of gastric cancer may have important significance.