在动物实验中根除幽门螺杆菌对萎缩性胃炎发生和逆转的影响

Hu Pin-jin, Zeng Zhirong, Li Hanliang, Chen Min-hu, Chen Wei, Peng Xiaozhong
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摘要

目的:在动物实验中探讨根除幽门螺杆菌对萎缩性胃炎发生和逆转的影响。方法:110只C57BL/6级雌性小鼠随机分为实验组(60只)和对照组(50只)。实验组小鼠感染SS1型幽门螺杆菌,随机分为A组和B组,每组30只。A组和B组分别在感染后6个月和12个月接受标准铋三联治疗。每组治疗前处死10只小鼠,治疗结束后3个月和6个月处死30只小鼠。采用类似Sydney系统的方法对腺胃的组织病理学特征进行分级,并采用抗brdu免疫组化染色和流式细胞术检测腺胃粘膜上皮细胞的动力学变化。结果:所有接受根除治疗的小鼠幽门螺杆菌检测均为阴性。A组和B组慢性活动性胃炎在根除幽门螺杆菌后均有明显改善。A组在任何时间间隔内均未见萎缩性变化,而B组在幽门螺杆菌感染后12个月出现萎缩性变化,在根除幽门螺杆菌后3个月和6个月萎缩程度无明显变化。实验组在根除幽门螺杆菌前的细胞动力学指标(s期细胞百分率、增殖指数和标记指数)在任何时间均显著高于对照组(P < 0.05)。结论:本研究提示,根除幽门螺杆菌可减轻胃黏膜炎症,改变胃上皮细胞动力学。发现早期治疗可预防粘膜萎缩的形成。当萎缩已经形成,根除幽门螺杆菌不能再扭转变化,但可能阻止其进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of eradicating Helicobacter pylori on the development and reversion of atrophic gastritis in an animal study
OBJECTIVE: To investigate the effect of eradicating Helicobacter pylori on the development and reversion of atrophic gastritis in an animal study. METHODS: One hundred and ten grade II C57BL/6 female mice were randomly divided into experimental (60 mice) and control (50 mice) groups. The mice in the experimental group were infected with the SS1 H. pylori strain, then randomly subdivided into group A and group B (30 mice in each group). Group A and group B received a dose of standard bismuth triple therapy 6 and 12 months after infection, respectively. Ten mice in each group were killed before the therapy, then at 3 and 6 months after completion of the therapy (a total of 30 mice). The histopathological features of the glandular stomach were graded using a method analogous to the Sydney system and kinetic changes in the mucosal epithelial cells of the glandular stomach were examined using anti-BrdU immunohistochemical staining and flow cytometry. RESULTS: All mice that received eradication therapy tested negative for Helicobacter pylori. Significant improvement in chronic active gastritis was observed after the eradication of H. pylori in both groups A and B. Atrophic changes were not seen at any time interval in group A, whereas in group B, atrophic changes were seen 12 months after H. pylori infection and no significant changes in the degree of atrophy were observed 3 and 6 months after the eradication of H. pylori. The cell kinetic indices (S-phase cell percentage, proliferation index and labeling index) in the experimental group before the eradication of H. pylori were significantly higher than those in the control group at any time (P 0.05). CONCLUSIONS: The present study suggests that the eradication of H. pylori can reduce gastric mucosal inflammation and change the epithelial cell kinetics of the stomach. It was found that early treatment can prevent the formation of mucosal atrophy. When atrophy has established, eradication of H. pylori can no longer reverse the change but may prevent its progress.
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