摘要
目的探讨姜黄素对结肠炎小鼠脾脏树突状细胞(DC)亚群及其表面活性分子的影响。方法雄性C57小鼠40只,随机分成正常组、200 mg/kg姜黄素组,300 mg/kg美沙拉嗪对照组。三硝基苯磺酸(TNBS)/乙醇法制备结肠炎小鼠模型。给药7 d后,处死小鼠,分离结肠测量其长度并称取其质量,取小鼠脾脏并分离DC,采用流式细胞术检测结肠炎小鼠CD205^+、CD4^+CD205^+、CD8^+CD205^+DC和表面分子主要组织相容性复合体Ⅱ(MHCⅡ)、Toll样受体2(TLR2)、TLR4、CD83的表达情况。同时观察其结肠病理损伤。结果经姜黄素治疗后,与模型组相比,结肠炎小鼠结肠质量指数明显下降,而结肠长度延长,病理性损伤明显缓解,同时其脾脏CD205^+、CD4^+CD205^+、CD8^+CD205^+DC亚群数量下降及其TLR2、TLR4、MHCⅡ的表达明显抑制,而CD83表达水平则显著增高。结论姜黄素治疗小鼠结肠炎可与调节结肠炎小鼠DC亚型比例及其表面共刺激分子的表达有关。
Objective To explore the effect of curcumin（ Cur） on the subpopulation and costimulatory molecules of dendritic cells（ DCs） in spleen from colitis mice. Methods Forty male C57/BL mice were randomly divided into 4 groups：normal group,model group,Cur group and mesalazine group. Colitis was induced by 2,4,6-trinitrobenzene sulfonic acid（ TNBS）. On the 8th day following 7-day treatment with Cur,the mice were sacrificed and the length and mass of mouse colon were measured. And then the spleens were separated to prepare DCs. The numbers of CD205^＋,CD4^＋CD205^＋,CD8^＋CD205^＋DCs and the levels of major histocompability complex Ⅱ（ MHC-Ⅱ）,Toll-like receptor 2（ TLR2）,TLR4 and CD83 expression were detected by flow cytometry. And we observed the pathological injury of colon. Results Compared with model group,the colonic mass index was reduced,the length of colon was lengthened,and the pathological injury was remitted.Meanwhile,the percents of CD205^＋,CD4^＋CD205^＋,CD8^＋CD205^＋DCs and the levels of MHC-Ⅱ,TLR2 and TLR4 were down-regulated,however,the CD83 expression was up-regulated. Conclusion Treatment efficacy of Cur on experimental colitis might be involved in regulating subpopulation and co-stimulatory molecules of dendritic cel s in spleen from mice with colitis.
出处
《细胞与分子免疫学杂志》
CAS
CSCD
北大核心
2016年第2期201-204,211,共5页
Chinese Journal of Cellular and Molecular Immunology
基金
国家自然科学基金(81460679
81260595)
2014年度国家留学基金委地方合作项目(201408360106
201408360110)
2015年度中医药科技计划项目(2015B049)
2015年江西中医药大学研究生校级课题(JZYC15S13)
