摘要
目的探讨晚期糖基化终产物(AGEs)对血管内皮细胞通透性的影响作用。方法将人脐静脉内皮细胞(HUVECs)与不同浓度的糖化牛血清白蛋白(AGE-BSA)共同培养8h,采用ELISA检测细胞培养上清中血管内皮钙黏蛋白(VE-cadherin)及金属基质蛋白酶(MMP9)的表达。然后将HUVECs与AGE-BSA100μg/ml及抗金属基质蛋白酶抗体(MMP9,MMP2)共同作用于单层内皮细胞8h后采用FITC荧光标记白蛋白漏出法测定单层内皮细胞通透率。结果与正常对照(NC)组相比,AGE-BSA 50、100μg/ml组细胞上清中VE-cadherin及MMP9含量明显升高(P<0.05或P<0.01)。与NC组相比,AGE-BSA组单层内皮细胞通透性增加(P<0.01);与AGE-BSA组相比,AGE-BSA+MMP9抗体组单层细胞通透性得到改善(P<0.05)。结论 AGE-BSA通过诱导MMP9激活,促进VE-cadherin自身解聚,从而导致内皮细胞通透性增高。
Objective To investigate the influence of advanced glycation end products （AGEs） to the permeability of vascular endothelial cell. Methods Human metalloproteinase 9 （MMP9） with ELISA assay. HUVECs were also treated with AGE-BSA （100 μg/ml） and MMPs antibody for 8 h, then FITC-albumin was added to evaluate Pvalue that reflects the permeability of endothelial monolayer. Results The levels of VE-cadherin and MMP9 were significantly increased in AGE-BSA 50 and 100/μg/ml groups than in NC group （P 〈 0. 01 or P 〈0. 05 ）. The permeability of HUVECs was significantly improved in AGE-BSA 100 μg/ml group,as compared with AGE-BSA 100 μg/ml ＋ MMP9 antibody （P〈 0.01）. Conclusion AGE-BSA can increase the permeability of vascular endothelial cell through inducing the activation of MMP9 and promoting the comolexion of VE-cadherin broke up.
出处
《中国糖尿病杂志》
CAS
CSCD
北大核心
2014年第5期464-466,共3页
Chinese Journal of Diabetes
基金
苏州市社会发展基金(SYS201127)
关键词
晚期糖基化终产物
血管内皮钙黏蛋白
内皮细胞通透性
金属基质蛋白酶
Advanced glycation end products
Vascular endothelial cell cadherin
Permeability oiendothelial cell~ Matrix metalloproteinase
