摘要
目的:探讨阿司匹林对胃溃疡愈合的影响和机制。方法:用乙酸诱导大鼠胃溃疡,然后随机分为模型对照组、生理盐水对照组、阿司匹林组。用组织学方法检测溃疡形态、溃疡面积和肉芽组织中的炎细胞数;用免疫组织化学方法检测核因子-κB、肿瘤坏死因子-α和白细胞介素-8在胃黏膜中的表达。结果:阿司匹林组的溃疡面积高于模型和生理盐水对照组(P<0.05);炎细胞数、核因子-κB、肿瘤坏死因子-α和白细胞介素-8的积分光密度都高于模型和生理盐水对照组(P<0.01)。结论:阿司匹林通过增加核因子-κB的表达上调肿瘤坏死因子-α和白细胞介素-8的表达,加重炎症反应,进而抑制溃疡愈合。
Objective: To explore the effects of aspirin on healing of gastric ulcer and pathogenesy. Methods: The gastric ulcers were induced with aeetie acid in rats and then the rats with the gastric ulcer were randomly divided into model control group, saline control group and aspirin group. The ulcerative appearanee, uleerative area and the number of inflammatory cells in granulation tissue were detected through histologieal method. The expressions of nuclear faetor-κB, tumor necrosis factor-α and interleukin-8 in gastric mueosa were detected through immunohistoehemieal method. Results: The ulcerative area in aspirin group was increased compared with that of model or saline control group (P〈0.05). The number of inflammatory cells, the integral light density of nuclear faetor-κB, tumor necrosis factor-α and interleukin-8 in aspirin group were increased compared with those of model or saline control group (P〈0.01). Conclusion: Aspirin up-regulate the expression of tumor necrosis factor-α and interleukin-8 by increasing the expressions of nuclear faetor-κB and then aggravateinflammatory reaction, which inhibit the ulcer healing.
出处
《中国医药导报》
CAS
2011年第23期16-17,21,共3页
China Medical Herald
基金
黑龙江省教育厅科学技术研究项目(项目名称:阿司匹林抑制溃疡愈合的分子机制
编号:11541416)
关键词
阿司匹林
溃疡愈合
炎症因子
Aspirin
Ulcer healing
Inflammatory factor