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作 者:钱冠清[1] 刘会齐[1] 刘春华[1] 刘晓辉[1] 吴其夏[2]
机构地区:[1]中国协和医科大学中国医学科学院血液学研究所,天津300020 [2]中国协和医科大学中国医学科学院基础医学研究所,北京100005
出 处:《基础医学与临床》2002年第6期517-520,共4页Basic and Clinical Medicine
基 金:国家自然科学基金重点项目 (39370 2 2 0 )
摘 要:探讨引起动脉粥样硬化 (AS)的一些有害因素作用脐静脉内皮细胞后 ,对单核细胞粘附率、VEC的白细胞粘附分子VCAM 1、ICAM 1及转录因子NFκB活化的影响 ,为阐明不同有害因素在AS早期发病机制中作用与机理提供依据。本文采用细胞计数法测粘附率 ,细胞免疫组化及ELISA法检测粘附分子表达及NFκB活化 ,原位杂交法测VCAM 1mRNA ;结果显示 ,mmLDL、rTNFα均能明显增加U937细胞的粘附 ,粘附百分率分别为对照组的 7倍和 9 2倍 ,rTNFα可使内皮细胞的VCAM 1、ICAM 1和P selectin表达显著上调 ,但mmLDL没有相似的作用 ;VEC在流体低剪切振荡流的作用下 ,明显上调VCAM 1mRNA及VCAM 1的表达 ,mmLDL、rTNFα和低剪切振荡流作用后 ,均可增加内皮细胞NFκB亚单位P6Focal recruitment of monocytes and lymphocytes is one of the earlist detectable cellular responses in the formation of atherosclerotic lesions(AS). To investigate the role of some risk factors in pathogenesis of AS, human Umbilical vein endothelial cells(HUVEC) were exposed to mmLDL,rTNF or low oscillatory shear stress and then the assay of cells adhesion percent, expression of leukocyte adhesion molecular VCAM 1 ICAM 1 P selectin and nuclear translocation of NFκB in HUVEC were examined by cell immunochemistry and hybridization in situ. The results indicated that U937 adhesion to HUVEC exposed to mmLDL or γTNF were 7.0fold and 9.0fold respectively as that of control(both P < 0.01). γTNF exposure induced hyperadherance by VCAM 1,ICAM 1,P selectin dependent mechanism. The cell surface expression of VCAM 1,ICAM 1in HUVEC was not increased after treatment with mmLDL. Low oscillory shear stress augments the expression of VCAM 1 both at protein and mRNA levels. Three risk factors elicited nuclear translocation of NFκB P65. The activation of endothelium NFκB by mmLDL, γTNF, low oscillory shear stress is a common signal pathway and may contribute to the formation of early atherosclerotic lesions.
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