糖尿病基础研究

　　　【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。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8 h，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-BSA100 μg/ml及抗金属基质蛋白酶抗体(MMP9，MMP2抗体)共同作用于单层内皮细胞8 h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<0.01或P<0.05)。与NC组相比，AGE-BSA组单层内皮细胞通透性增加明显(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。

　　【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

　　　【Abstract】 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 (100μg/ml) and MMPs antibody for 8 h, then FITC-albumin was added to evaluate P value that reflects the permeability of endothelial monolayer. Results The levels of VE-cadherin and MMP9 were significantly increased in AGE-BSA 50 and 100μg/ml groups than i P<0.01 or P<0.05). The permeability of HUVECs was significantly improved in AGE-BSA 100μg/ml group, as compared with AGE-BSA 100 μg/ml + MMP9 antibody (P< 0.01). Conclusions AGE-BSA can increase the permeability of vascular endothelial cell through inducing the activation of MMP9 and promoting the complexion of VE-cadherin broke up.

　　【Key words】Advanced glycation end products; Vascular endothelial cell cadherin; Permeability of endothelial cell; Matrix metalloproteinase normal group