黄芪多糖对淋巴细胞与血管内皮细胞粘附的影响及其分子机制  

Effect of astragalus polysaccharin(APS)on lymphocyte-endothelium adhesion and the molecular mechanism

作　　者：郝钰[1] 邱全瑛[1] 吴珺[1] 

机构地区：[1]北京中医药大学微生物学与免疫学教研室,北京100029

出　　处：《免疫学杂志》2000年第3期206-209,共4页Immunological Journal

基　　金：国家自然科学基金!(39870949);教委博士点基金!(9858)资助项目

摘　　要：目的从影响淋巴细胞与血管内皮细胞粘附的角度探讨黄芪多糖免疫增强作用的机制。方法以体外培养的人脐静脉内皮细胞 ( HU VEC)为模型 ,应用蛋白染料染色、细胞 EL ISA、免疫细胞化学等方法 ,研究黄芪多糖对淋巴细胞与血管内皮细胞粘附的影响及其分子机制。结果黄芪多糖作用于 HUVEC,能促进 HUVEC与淋巴细胞粘附 ,并与 IL - 1、TNF有协同增强作用 ,其主要分子机制为促进 HU VEC表面粘附分子 ICAM- 1的表达 ;黄芪多糖作用于淋巴细胞 ,不增强淋巴细胞与HUVEC粘附 ,同时也不提高淋巴细胞表面粘附分子 CD18的表达。结论通过提高细胞表面粘附分子的表达而促进淋巴细胞与内皮细胞的粘附 。ObjectiveTo investigate the effect of APS on lymphocyteendothelium adhesion and cell adhesion molecules(CAMs)Methods Based on the model of human umbilical vein endothelial cell(HUVEC),this study adopted Rose Bengal Stain,cell ELISA,immunocytochemistry techniques to investigate the effect of APS on lymphocyteendothelium adhesion and the molecular mechanismResults Incubation of HUVEC with APS markedly enhanced HUVEC adherence for lymphocyte and APS had synergism with IL1 and TNFThe main molecular mechanism is that APS upregulate the expression of ICAM1 on the HUVECThe lymphocyte treated with APS did not show increase in their adherence to HUVEC,and had no upregulation of CD18 expressionConclusion It is one of the mechanisms of immunopotentiation of APS that it promote lymphocyteendothelium adhesion by upregulating the CAMs expression to promote lymphocyte recirculation [

关 键 词：黄芪多糖 淋巴细胞 血管内皮细胞 粘附分子 

分 类 号：R285[医药卫生—中药学]