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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
Objective: To study the dynamic changes of serum IL-6 and IL-8 in rats with atrophic gastritis caused by hot saline and to discuss the relationship between long-term hot and salty diet and atrophic gastritis. Methods: Animal models of atrophic gastritis in rats were established by intragastric administration of hot saline. The contents of IL6 and IL-8 in the serum of 4, 8, 12, 24 and 32 weeks after the normal diet, normal control group and experimental group were detected by ELISA. Results: Gastric mucosa became thinner at 12wk, the glandular lamina propria of the lamina propria was reduced, connective tissue hyperplasia of lamina propria, hyperplasia of muscularis mucosa and chronic atrophic gastritis infiltration were observed. Prolonged, 32wk gastric mucosal atrophy significantly increased; normal control group and normal feeding group at each time point serum IL-6, IL-8 content is basically the same. The content of IL-6 in the experimental group increased significantly at 4wk, while the levels of IL-6 at 8 and 12wk remained at a relatively high level, which was significantly different from that of the normal control group; it dropped to normal after 24wk. The content of IL-8 also significantly higher than the normal control group at 4 and 8 weeks; after 12 weeks of atrophic gastritis, its content decreased to normal. Conclusions: In the early period of atrophic gastritis caused by hot salt water, the serum levels of IL-6 and IL-8 were significantly increased. The inflammation mediated by IL-6 and IL-8 may be caused by the early thermal saline damage of gastric mucosa One of the main mechanisms plays an important leading role in the formation of atrophic gastritis