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作 者:翟金海[1] 沈洪[2] 倪菲菲[1] 朱磊[2] 刘智群[1]
机构地区:[1]南京中医药大学第一临床医学院,南京210046 [2]江苏省中医院消化内科,南京210029
出 处:《中国中西医结合杂志》2012年第10期1366-1369,共4页Chinese Journal of Integrated Traditional and Western Medicine
基 金:国家自然科学基金资助项目(No.81072778);江苏省自然科学基金资助项目(No.BK2011078);江苏高校优势学科建设工程资助项目(No.B222)
摘 要:目的观察清肠化湿方对实验性大鼠结肠炎树状突细胞(dendritic cells,DCs)的影响,以探讨其治疗溃疡性结肠炎(ulcerative colitis,UC)的可能机制。方法采用三硝基苯磺酸(TNBS)/无水乙醇诱导大鼠结肠炎模型,40只雄性Wistar大鼠随机分为正常组、模型组、清肠化湿方组和美沙拉嗪组,每组10只。造模后第2天,用药组分别给予相应药物连续灌胃10天。免疫组化法观察大鼠结肠黏膜DCs数目;流式细胞仪检测肠系膜淋巴结DCs比例及表面分子MHC-Ⅱ和CD86表达。结果与模型组比较,清肠化湿方组和美沙拉嗪组大鼠结肠黏膜DCs数目显著减少,肠系膜淋巴结MHC-Ⅱ表达显著降低,差异均有统计学意义(P<0.01);两用药组比较,差异无统计学意义(P>0.05)。各组DCs比例和CD86表达比较,差异均无统计学意义(P>0.05)。结论减少结肠黏膜DCs浸润,抑制肠系膜淋巴结DCs的活化,是清肠化湿方治疗UC的机制之一。Objective To observe the effects of Qingchang Huashi Recipe (QHR) on the dendritic cells (DCs) of experimental colitis rats, thus exploring its possible mechanisms for treating ulcerative colitis (UC). Methods The UC rat model was induced by TNBS/anhydrous alcohol. Forty male Wistar rats were randomly di- vided into 4 groups, i.e., the normal group, the model group, the QHR group, and the Mesalazine group, 10 in each group. Since the 2nd day of modeling, corresponding medication was respectively administered to each treatment group by gastrogavage for 10 successive days. The number of DCs in the colonic mucosa was ob- served using immunohistochemical assay. The DCs ratio in the mesenteric lymph nodes, and the expressions of surface molecules MHC-]] and CD86 were detected using flow cytometry. Results Compared with the model group, the number of DCs in the colonic mucosa significantly decreased, the expression of MHC- 11 in the mesen- teric lymph nodes significantly decreased in the QHR group and the Mesalazine group, showing statistical differ- ence (P〈0.01). There was no statistical difference between the two groups (P〉0.05). There was no statisti- cal difference in the DCs ratios and the CD86 expression among the 4 groups ( P 〉 0.05). Conclusion QHR could decrease the infiltration of DCs in the colonic mucosa, and suppress the activation of DCs in the mesenteric lymph nodes, which might be one of its mechanisms for treating UC.
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