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不同毒力的幽门螺杆菌对溃疡愈合的影响及机制
引用本文:王化冰,DONG Xiu-yun,董秀云. 不同毒力的幽门螺杆菌对溃疡愈合的影响及机制[J]. 北京大学学报(医学版), 2001, 33(3): 263-265
作者姓名:王化冰  DONG Xiu-yun  董秀云
作者单位:^A北京大学第三医院消化内科;北京医院消化科^B北京大学医学部附属第三医院(北医三院)^C1447^D1%^ADepartment of Gastroenterology, Peking University Third Hospital,^B北京大学医学部附属第三医院(北医三院)^C1447^D2%^A北京大学第三医院消化内科,^B北京大学医学部附属第三医院(北医三院)^C1447^D3
摘    要:目的:观察不同毒力的幽门螺杆菌( Helicob acter pylori , Hp)对大鼠溃疡愈合过程的影响,并初步探讨其机制。方法:以50%(体积分数)乙酸烧灼大鼠浆膜面的方法制备胃溃疡模型,经口灌服不同毒力的Hp菌液,14 d后测定溃疡指数,并通过放免法、酶免法以及免疫组化的方法分别测定血清胃泌素和白细胞介素8(interleukin-8,IL-8)含量、胃黏膜D细胞染色强度和密度。结果:实验组与对照组比较,前者溃疡指数、血清胃泌素和IL-8 含量均高于后者,而D细胞染色强度和密度低于后者。VacA +组与VacA -组比较,前者溃疡指数、血清胃泌素含量高于后者,D细胞染色强度和密度低于后者,IL-8水平两者差异无显著性。结论:经口灌服Hp 菌液可延迟大鼠溃疡愈合时间,且VacA + 菌株较VacA -菌株延迟愈合作用更加明显,H p延迟溃疡愈合的机制可能与增高血清胃泌素含量、减少胃黏膜生长抑素的分泌、提高血清IL-8 水平有关。

关 键 词:螺杆菌  幽门  胃溃疡/微生物学  胃泌素类/血液  生长抑素/分泌  白细胞介素8/血液  
文章编号:1671-167X(2001)03-0263-03

The effect of Helicobacter pylori with different virulence on the healing pr ocess of ulcer and its mechanism of action
WANG Hua Bing,DONG Xiu Yun. The effect of Helicobacter pylori with different virulence on the healing pr ocess of ulcer and its mechanism of action[J]. Journal of Peking University. Health sciences, 2001, 33(3): 263-265
Authors:WANG Hua Bing  DONG Xiu Yun
Abstract:To observe the effect of Helicobacter pylori ( H. pylori ) with different virulence on the healing process of ulcer in rats and to investigate the mechanism. Methods: By preparing the models of acetic acid induced gastric ulcer in rats and giving them H. pylori strains with different virulence orally, the ulcer index was determined after 14 days. Furthermore, the methods of radioimmunoassay, ELISA and immunohistochemical staining were used to determine the content of serum gastrin and IL 8 and to evaluate D cell intensity and density in gastric mucosa. Results: The ulcer index, the content of serum gastrin and IL 8 in the test groups were found to be higher than those of the control, but the D cell intensity and density in the test groups were significantly reduced compared with the control. The ulcer index and the content of serum gastrin in VacA + group were higher than those of VacA - group, but the D cell intensity and density in VacA + group were reduced compared with VacA - group and there was no significant difference on serum IL 8 level between VacA + group and VacA - group. Conclusion: The healing process of gastric ulcer was delayed by giving H. pylori strains orally. The delaying effect was even more obvious in VacA + strain compared with VacA - strain. The mechanism involved in delaying ulcer healing by H. pylori might include reduction of D cell density and intensity and increase of serum gastrin and IL 8 level.
Keywords:Helicobacter pylori  Stomach ulcer/microbiol  Gastrins/blood  Somatostatin/secret  Interleukin 8/blood
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