摘要
目的观察不同强度恒磁场对糖基化终产物(AGE)作用下人脐静脉内皮细胞(HUVEC)分泌细胞间黏附分子-1(ICAM-1)及HUVEC与人单核细胞株THP-1黏附的影响。方法采用体外培养第3代的HUVEC,实验分为6组,即对照组、AGE组(AGE-BSA100μg/L)及AGE+不同强度(1、5、10、20Gs)的恒磁场组。各组细胞于培养及恒磁场作用24h后收集标本,用酶联免疫吸附试验(ELISA)检测HUVEC分泌I-CAM-1的量,计数法观察HUVEC与THP-1的黏附率。结果AGE组细胞ICAM-1的分泌量显著增高(P<0.05vs对照组),而1、5、10和20Gs恒磁场组细胞ICAM-1的分泌量显著低于AGE组(P<0.05)。AGE组HUVEC与THP-1的黏附率显著增加(P<0.05vs对照组),而1、5、10和20Gs恒磁场组HUVEC与THP-1的黏附率显著低于AGE组(P<0.05)。结论1-20Gs的恒磁场可拮抗AGE的作用,抑制HUVEC分泌ICAM-1及与单核细胞的黏附率。
[Objective]To investigate effects of constant magnetic field on secretion of intercellular adhesion molecule-1 (ICAM-1) by human umbilical vein endothelial cells(HUVEC) and their adhesion with monocytes (THP-1) induced by advanced glycosylation endproduct (AGE). The third passage of cultured HUVEC was used. The cells were divided into six groups, i. e, control group, AGE group, AGE with one, five, ten or 20 gausses of constant magnetic field group.Samples were collected 24 hours later. Secretion of ICAM-1 was detected by ELISA and the adhesion rates between HUVEC and THP-1 were measured by counting method. Secretion of ICAM-1 significantly increased 24 hours after intervention by AGE of 100μg/L (P <0.05 vs control). Wheras in one, five, ten and 20 gausses group, secretion of ICAM-1 significantly decreased comparing with the AGE group (P <0.05). The adhesion rates between HUVEC and THP-1 significantly increased 24 hours after incubation of HUVEC with AGE (P <0.05 vs control). Wheras in 1, 5, 10 and 20 gausses group, the adhesion rates between HUVEC and THP-1 significantly decreased comparing with the AGE group (P <0.05). [Conclusion] One gauss to 20 gausses of constant magnetic fields can intensity-dependently antagonize effects of AGE on HUVEC,i.e, decreasing secretion of ICAM-1 by HUVEC and the adhesion rates between HUVEC and THP-1.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2005年第9期1301-1304,共4页
China Journal of Modern Medicine
基金
国家自然科学基金资助项目(30270396)
关键词
恒磁场
糖基化终产物
内皮细胞
单核细胞
细胞间黏附分子-1
constant magnetic field
advanced glycosylation endproduct
endothelial cells
monocyte
intercellular adhesion molecule-1