中文摘要：

目的：观察晚期糖基化终产物（AGEs）对足细胞整合素连接激酶的影响及可能机制。方法：不同浓度的AGEs干预小鼠足细胞，分别检测足细胞整合素连接激酶（ILK）的表达、足细胞黏附性和足细胞上清血管紧张素Ⅱ的浓度，然后预氯沙坦（100 μmol）预处理足细胞后，观察足细胞ILK和黏附性的变化。结果：AGEs（80 μg／ml）干预足细胞24h可明显上调ILK的表达[（200±22）％vs.100％，P〈0.05]，降低足细胞的黏附性[（40±13）％vs.100％，P〈0.05]，同时升高细胞上清中血管紧张素Ⅱ的浓度[（11.2±0.8）vs.（7.0±0.7）ps／ml，P〈0.05]，而氯沙坦预处理可减轻AGEs介导的ILK的上调[（124±25）％vs.（2004±22）％，P〈0.05]，足细胞的黏附性也明显改善[（75±13）％VS.（40±13）％，P〈0.05]。结论：AGEs可能通过激活足细胞内的肾素-血管紧张素系统，上调足细胞ILK的表达，降低足细胞的黏附性。

英文摘要：

Objective：To investigate the effects and mechanism of advanced glycation end products （AGEs） on the expression of integrin linked kinase（ILK） in podocytes. Methods ：Immortalized mouse podocytes were exposed to different concentrations of AGEs, expression levels of ILK protein were measured by western blot, podocyte adhesion was evaluated by hexosaminidase assay, angiotensin Ⅱ levels were measured by enzyme - linked immunosorbent assay. Then podocytes were pretreated with angiotensin Ⅱ type 2 receptor losartan, the changes of ILK and podocyte adhesion were observed. Results： Treatment with AGEs （ 80 μg/ml） for 24 hours resulted in an incremental rise in ILK expression up to an increase of 100% and a significant, dose -dependent decrease in podocyte adhesion [（40 ± 13）% vs. 100%, P 〈0.05] . AGEs also increased angiotensin I1 levels significantly[（11.2 ±0.8） vs. （7.0 ±0.7） pg/ml,P 〈 0.05]. Pretreatment with losartan significantly prevented the upregulation of ILK [（124±25 ） % vs. （200±22 ） %, P 〈 0.05 ] and improved podocyte adhesion compared with podocytes exposed to AGEs [ （75 ± 13 ） % vs. （40 ± 13） % ,P 〈 0.05]. Conclusion：Our findings indicate that AGEs upregulate ILK expression, which occurres partly through activation of the renin - angiotensin system in podocytes.