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作 者:肖源[1] 车筑平 杨红静[3] 程华[1] 谭庆华[4]
机构地区:[1]贵阳医学院第三附属医院消化内科,558000 [2]附属医院内镜中心,550004 [3]贵阳医学院第三附属医院临床医学系,558000 [4]四川大学华西医院消化内科,成都610041
出 处:《免疫学杂志》2015年第9期786-789,共4页Immunological Journal
基 金:贵州省科技厅基金(E2011-10)
摘 要: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。To investigate the changes of ileal sIgA, dendritic cells and plasma cells in SD rat with non- steroidal anti-inflammatory drugs (NSAIDs) enteropathy, total of 34- SPF grade Sprague-Dawley rats, males and females, aging 8 weeks, weighing 200-220 g, were randomly divided into 2 groups with 17 rats in each group. The aspirin group received intraperitoneal injections of 100 mg/kg aspirin twice daily for 14 days, while the control group received equal volume of normal saline. 5 cm from the ileocecal valve in the proximal intestine was cut off by 2 cm, to detect the level of sIgA by ELISA, and the quantity of CD205-positive and CD38-positive cells in mucosa by immunohistochemistry analysis. Compared with control group, the level of sIgA in ileal tissue of aspirin group decreased (P〈 0.05), while the number of dendritic cells and plasma cells increased (P〈 0.01). In conclusion, the increase of dendritic cells and plasma cells in NSAIDs-induced enteropathy suggested the acquired immune responses in the intestinal were induced. However, reduction of sIgA levels in ileal tissue could be related with depression of IgA synthesis or impaired synthesis of secretory components or both, and most likely to occur in the IgA and SC in epithelial cells during assembly process. Taken together, NSAIDs-induced enteropathy not only damages the intestinal mucosa but also causes acquired immune responses disorders.
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