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目的探讨幽门螺杆菌（Ｈｐ）感染对胃癌癌前病变细胞凋亡的影响。方法采用原位切口末端标记方法检测细胞凋亡，平均每１００个细胞内的阳性细胞数为凋亡指数（ＡＩ）。结果肠化生和异型增生粘膜的ＡＩ分别为３．４±０．９％和１．４±０．７％，明显低于慢性胃炎（６．０±１．８％）（Ｐ值均小于０．０１）；Ｈｐ阳性肠化生和异型增生的ＡＩ分别为３．７±１．１％和１．５±０．７％，与Ｈｐ阴性肠化生（３．１±０．７％）和异型增生（１．３±０．４％）相比差异无显著性（Ｐ值均大于０．０５）。结论胃癌癌前病变粘膜细胞存在凋亡抑制，尽管Ｈｐ感染可诱导胃上皮细胞凋亡，但可能对肠化生和异型增生的细胞凋亡无影响。
Objective To investigate the effect of Helicobacter pylori (Hp) infection on the apoptosis of gastric precancerous lesions. Methods Apoptosis was detected by in situ nick end labeling. The average number of positive cells per 100 cells was apoptosis index (AI). Results AI in intestinal metaplasia and dysplasia mucosa were 3.4 ± 0.9% and 1.4 ± 0.7% respectively, which were significantly lower than those in chronic gastritis (6.0 ± 1.8%) (P < 0.01). The AI of Hp positive intestinal metaplasia and dysplasia were 3.7 ± 1.1% and 1.5 ± 0.7% respectively, which was significantly higher than that of Hp negative intestinal metaplasia (3.1 ± 0.7% ) And dysplasia (1.3 ± 0.4%) compared with no significant difference (P values were greater than 0.05). Conclusion The gastric mucosal cells in gastric precancerous lesions exist inhibition of apoptosis, although Hp infection can induce gastric epithelial cell apoptosis, but may have no effect on intestinal metaplasia and dysplasia of apoptosis.