摘要
目的既往实验已观察到糖基化终产物(advanced glycation end products,AGEs)可增加人肾系膜细胞(human renal mesangial cell,HRMC)Fractalkine(FKN)mRNA和蛋白的表达,现进一步探讨AGEs对HRMC FKN的趋化功能及分泌的影响。方法运用体外制备的糖基化修饰的牛血清白蛋白(AGE-bovine serum albumin,AGE-BSA)干预HRMC,用Transwall小室装置检测HRMC趋化单核细胞的功能,用ELISA法检测HRMC上清液中FKN的蛋白含量。结果1.AGE-BSA组HRMC趋化单核细胞数显著高于对照组,FKN中和抗体组HRMC趋化单核细胞数较AGE-BSA组显著减少;2.随着AGE-BSA浓度的增高及干预时间的延长,细胞的FKN蛋白分泌水平随之增高,且显著高于对照组(P<0.01)。结论AGE-BSA可增强HRMC趋化单核细胞的功能,此效应可被FKN中和抗体部分抑制,且AGE-BSA呈时间和浓度依赖性增加HRMC FKN的蛋白分泌,提示AGEs可能部分通过FKN途径参与糖尿病肾病的发生发展。
Objective To investigate the effects of advanced glycosylation end products （AGEs） on the capacity of fractalkine （FKN） inducing monocytes transmigration to the cultured human renal mesangial cells （HRMC） and the secretion of FKN in HRMC. Methods AGEs were prepared by incubation of bovine serum albumin （BSA） with high concentration of glucose at 37℃ for conditioned time in vitro. HRMC was cultured in the presence of AGE - BSA. The capacity of FKN to induce monocytes transmigration was detected with a Transwell system. The concentration of FKN in the supernatant was quantified by ELISA. Results 1. In AGE - BSA group, the number of monocytes migrated to HRMC was higher than control groups and anti - FKN antibody - blocking group （ P 〈 0. 01）. 2. After incubation of HRMC with AGE -BSA, the content of FKN in supernatant was significantly increased compared with that in control group in dose and time dependent manner （ P 〈0.01）. Conclusion AGEs stimulate FKN secretion and monocyte migration which is partly inhibited by anti - FKN Ab. These findings suggest that FKN might mediate the role of AGEs in the development of diabetic nephropathy.
出处
《中国微循环》
北大核心
2008年第4期202-205,共4页
Journal of Chinese Microcirculation
基金
江苏省科技厅重大招标项目(BS2003056)
江苏省中医药管理局科技基金(H05119)
