血清IL-6,IL-8在热盐水致大鼠萎缩性胃炎发生发展过程中的作用

目的:研究热盐水灌胃导致的大鼠萎缩性胃炎血清IL-6,IL-8含量的动态变化,探讨长期热咸饮食与萎缩性胃炎发生的关系。方法:用热盐水灌胃建立大鼠萎缩性胃炎动物模型,用ELISA方法检测正常喂养组、正常对照组和实验组4,8,12,24,32wk血清IL6,IL-8含量的动态变化。结果:灌胃至12wk时出现胃粘膜层变薄,固有层腺体减少,固有层纤维结缔组织增生,粘膜肌层明显增生,慢性炎细胞浸润等萎缩性胃炎表现,随着热盐水灌胃时间的延长,32wk胃粘膜萎缩程度明显加重;正常对照组和正常喂养组大鼠各时间点血清IL-6,IL-8含量基本相同。实验组大鼠血清IL-6含量在4wk就明显升高,8,12wkIL-含量仍保持在较高水平,与正常对照组相比,有显著差异性;24wk后降至正常。IL-8含量在4,8wk也明显高于正常对照组;12wk萎缩性胃炎形成后,其含量降至正常。结论:热盐水导致大鼠萎缩性胃炎形成的较早时期,血清IL-6,IL-8含量明显升高,IL-6,IL-8所介导的炎症可能是早期热盐水损伤胃粘膜的主要机制之一,在萎缩性胃炎形成中起重要的先导作用

Serum IL-6 and IL-8 in pathogenesis of atrophic gastritis cused by high-salt hot diet

Objective: To measure the IL-6,IL-8 in blood serum of atrophic gastritis caused by high-salt-hot water in rats and to study the pathogenesis of atrophic gastritis caused by high-salt-hot diet. Methods: The atrophic gastritis rat model was made by high-salt-hot water in perfusion. The IL-6 and IL-8 level in blood serum in 4,8,12,32wk in rat were tested by EILSA. Results: All rats in experiment group devloped CAG at the end of 12 weeks with the following Pathological changes of CAG such as thin mucosa layer,thick muscle layer,decreased glandes,soakaging inflammation cells in microscope and with the time prolonging, the atrophy of gastric mucosa became more serious;In normal control group and normal feeding group ,the IL-6 and IL-8 content in blood serum are the same at every time point ; In experiment group , IL-6 became increased from 4wk and kept high level from 4wk to 12wk and had significant difference compared with normal controls. In 24wk the level of IL-6 has no significant difference compare with normal controls. IL-8 level became increased from 4wk and 8wk, and had significant difference compared with normal controls. In 12wk while CAG was formed, the level of IL-8 had no significant difference compared with normal controls.Conclusion: In early time of CAG formation caused by high salt hot water, the level of IL-6 and IL-8 in rats' blood serum increased significantly. They may play an important precursor role in high salt hot water induced gastric mucosa and in the formation of CAG.