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目的 明确根除幽门螺杆菌 (Helicobacterpylori,Hp)对萎缩性胃炎的形成和逆转的影响。方法 110只 2级C57BL/ 6小鼠随机分为实验组 (6 0只 )和对照组 (5 0只 )。实验组动物感染Hp后又随机分为A、B两组 ,并分别于感染后 6个月和 12个月根除Hp。采用悉尼系统、免疫组化及流式细胞术比较根除前后鼠腺胃黏膜组织学和细胞动力学。结果 (1)接受根除治疗的动物Hp检查均为阴性。根除Hp可明显改善A、B两组动物腺胃的慢性活动性炎症。A组动物在各时间点均未观察到萎缩的形成 ,B组动物于感染Hp后 12个月腺胃出现萎缩性改变 ,根除Hp后 3个月、6个月萎缩未有明显减轻。(2 )根除Hp可明显改善腺胃黏膜细胞动力学 ,根除后 6个月时S期细胞百分比 (S % )、增殖指数 (PI)和胃黏膜上皮细胞Brdu标记指数 (LI)与同期对照组动物比较差异无显著性 (P值均 >0 .0 5 )。结论 本研究表明 ,早期根除Hp可预防萎缩性胃炎的形成 ,对已形成的萎缩性胃炎无逆转作用 ,但可防止病变进一步发展
Objective To clarify the effect of Helicobacter pylori (Hp) on the formation and reversal of atrophic gastritis. Methods One hundred and two Grade 2 C57BL / 6 mice were randomly divided into experimental group (60) and control group (50). The experimental animals were infected with Hp and then randomly divided into A and B groups. Hp was eradicated at 6 and 12 months after infection respectively. The gastric mucosa histology and cell kinetics of edema rats were compared using Sydney system, immunohistochemistry and flow cytometry. Results (1) All the animals undergoing eradication therapy had negative Hp test. Eradication of Hp can significantly improve chronic active inflammation in the gland and stomach of A and B groups. In group A, no atrophy was observed at all time points. In group B, the atrophy of glandular and stomach was observed 12 months after infection with Hp, but there was no significant reduction at 3 and 6 months after Hp eradication. (2) The eradication of Hp could significantly improve the glandular mucosal cell kinetics. The percentages of S phase, proliferation index (PI) and Brdu labeling index (LI) in gastric mucosal epithelial cells at 6 months after eradication were significantly higher than those in the control group There was no significant difference between animals (P> 0.05). Conclusions This study showed that early eradication of Hp prevented the formation of atrophic gastritis and did not reverse the atrophic gastritis that has developed, but prevented further development of the disease