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目的 :观察不同毒力的幽门螺杆菌 (Helicobacterpylori,Hp)对大鼠溃疡愈合过程的影响 ,并初步探讨其机制。方法 :以 5 0 % (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 ,14d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 ,Hp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
Objective: To observe the effect of different virulence of Helicobacter pylori (Hp) on the healing process of ulcer in rats, and to explore its mechanism. Methods: Gastric ulcer model was prepared by cauterizing serous surface of rats with 50% acetic acid. After oral administration of Hp strain with different virulence, the ulcer index was determined 14 days later. Immunohistochemistry was used to determine the levels of serum gastrin and interleukin 8 (IL 8) and the staining intensity and density of gastric mucosal D cells respectively. Results: Compared with the control group, the ulcer index, serum gastrin and IL-8 in the experimental group were higher than those in the control group, while the staining intensity and density of D cells were lower than those in the control group. Compared with the VacA-VacA-group, the former had higher ulcer index and serum gastrin than the latter, and the staining intensity and density of D cells were lower than those of the latter. There was no significant difference between the two groups in the level of IL-8. Conclusion: The oral administration of Hp bacteria can delay the healing time of ulcer in rats, and VacA + strains delayed the more obvious effect of VacA-strain. The mechanism of Hp delayed ulcer healing may be related to increasing serum gastrin and reducing gastric mucosal growth Hormone secretion, increase the level of serum IL 8