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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 effect of advanced glycation end products (AGEs) on the permeability of vascular endothelial cells. Methods Human umbilical vein endothelial cells (HUVECs) were cultured with different concentrations of AGE-BSA for 8 h. The expression of VE-cadherin and metalloproteinases (MMP9) expression. HUVECs were treated with AGE-BSA100μg / ml and anti-MMP-9 (MMP9, MMP2) for 8h, then the permeability of monolayer endothelial cells was measured by FITC fluorescent albumin leakage assay. Results Compared with NC group, the levels of VE-cadherin and MMP9 in AGE-BSA 50,100μg / ml group were significantly increased (P <0.05 or P <0.01). Compared with NC group, the permeability of monolayer endothelial cells in AGE-BSA group increased (P <0.01). Compared with AGE-BSA group, the permeability of monolayer cells in AGE-BSA + MMP9 group was improved (P < 0.05). Conclusion AGE-BSA can promote endothelial cell permeability by inducing the activation of MMP9 and promoting the depolymerization of VE-cadherin.