【摘要】目的 探讨玉葵清对糖基化终产物(AGEs)诱导的人肾系膜细胞(HRMC)趋化因子表达及其趋化效应的影响。 方法 糖基化牛血清白蛋白(AGE- BSA)和玉葵清干预HRMC。 结果 AGE- BSA组较BSA组HRMC趋化单核细胞数增加，MCP-1、Fractalkine中和抗体组HRMC趋化单核细胞数较AGE-BSA组减少;玉葵清组MCP-1、Fractalkine基因表达、上清中的蛋白含量和趋化单核细胞较BSA组降低(P<0.05)。结论 玉葵清减弱AGE- BSA诱导的HRMC趋化因子表达及其趋化效应，可能改善糖尿病肾病肾脏炎症反应。

　　【关键词】糖基化终产物;MCP-1;fractalkine;玉葵清;糖尿病肾病

　　【Abstract】Objective To further investigate the effect of YuKuiQing on the upregulation of monocyte chemoattractant protein-1 (MCP-1) and fractalkine (FKN) induced by AGEs. Methods Human renal mesangial cells (HRMC) was cultured in the presence of AGE-BSA with or without anti-MCP-1 and anti-FKN antibody or YuKuiQing. The capacity of MCP-1 and FKN to induce monocytes transmigration was detected with a Transwell system. The MCP-1 and FKN mRNA and protain in HRMC were analyzed by RT-PCR and ELISA. Results 1.The number of monocytes migrating to HRMC was higher in AGE-BSA group than in control and anti-MCP-1 or anti-FKN antibody-blocking groups(P<0.01). 2. The number of monocytes migrating to HRMC was lower of YuKuiQing than in control and AGE-BSA (P<0.01)group. 3. Expression of MCP-1 and FKN mRNA significantly lower in YuKuiQing group than in control group (P<0.01) and AGE-BSA(P<0.05) group. 4. In YuKuiQing group, the contents of MCP-1 and FKN in supernatant were significantly decreased compared to control and AGE-BSA groups (P<0.01). Conclusions 1. AGE-BSA enhances the capacity of MCP-1 and FKN to induce monocytes transmigration to HRMC, which are inhibited by anti-MCP-1 and anti-FKN antibody partially. These findings suggest that MCP-1 and FKN might mediate the role of AGEs in the development of diabetic nephropathy. 2. YuKuiQing can markedly reduce the upregulation of MCP-1 and FKN induced by AGE-BSA, and attenuate the capacity of MCP-1 and FKN to induce monocytes transmigration to HRMC. These results indicate that YuKuiQing might play its role of renal protection.

　　【Key words】 Advanced glycation end products; MCP-1;Fractalkine; YuKuiQing; Diabetic nephropathy