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目的探讨非甾体类消炎药(non-steroid anti-inflammatory drugs,NSAIDs)引起肠病时SD大鼠回肠s Ig A、树突状细胞、浆细胞的变化。方法清洁级SD大鼠34只,雌雄各半,年龄8周,体质量200~220 g,分为药物损伤模型组(阿司匹林组)和对照组(生理盐水组),每组17只。药物损伤模型组腹腔注射阿司匹林,100 mg/kg,每天2次;对照组腹腔注射等量生理盐水,每天2次。2周后处死大鼠,在距回盲瓣5 cm近端肠管切取回肠段2 cm。ELISA法检测回肠组织s Ig A水平,免疫组化法检测回肠组织CD205、CD38阳性染色细胞数量。结果阿司匹林组与对照组比较,阿司匹林注射组大鼠回肠黏膜s Ig A降低(P<0.05),树突状细胞和浆细胞数量增多(P<0.01)。结论 NSAIDs肠病发生后,树突状细胞和浆细胞数量增多,这提示肠道发生适应性免疫反应。但最终肠道黏膜内s Ig A分泌明显较少,这可能与分泌型Ig A形成过程受损相关,最可能发生在Ig A与SC在上皮细胞内装配的过程中。这说明,NSAIDs肠病不仅损害肠黏膜屏障,还可致体液免疫紊乱。
Objective To investigate the changes of s Ig A, dendritic cells and plasma cells in SD rats during enteropathy caused by non-steroid anti-inflammatory drugs (NSAIDs). Methods Thirty-four SD rats were divided into two groups: male and female, aged 8 weeks and weight ranging from 200 to 220 g. They were divided into two groups: drug-induced injury model group (aspirin group) and control group (saline group), 17 rats in each group. The model of drug injury was injected aspirin 100 mg / kg intraperitoneally twice a day. The control group was given intraperitoneal injection of normal saline twice a day. After 2 weeks, the rats were sacrificed, and the ileum segment was excised 2 cm proximal to the ileocecal valve 5 cm. ELISA method was used to detect the level of s Ig A in ileum. The number of CD205 and CD38 positive cells in ileum was detected by immunohistochemistry. Results Compared with the control group, the s Ig A of ileum mucosa in aspirin injection group decreased (P <0.05) and the number of dendritic cells and plasma cells increased (P <0.01). Conclusions After the onset of NSAIDs enteropathy, the number of dendritic cells and plasma cells increased, suggesting an adaptive immune response in the intestine. However, the final intestinal mucosal s Ig A secretion was significantly less, which may be associated with impaired secretory Ig A formation, the most likely occurs in Ig A and SC in the process of epithelial cell assembly. This shows that NSAIDs enteropathy not only damage the intestinal mucosal barrier, but also cause humoral immune disorders.