中文摘要：

目的探讨整合素连接激酶（ILK）对高浓度葡萄糖诱导的人晶状体上皮细胞（LECs）增生和转化的作用。方法将体外培养的人LECs系SRA01/04细胞分别培养在含葡萄糖5.5mmol/L（正常对照组）和30.5mmol/L（高糖组）的培养液中,用RT-PCR检测培养0、6、24h后ILK mRNA的表达;用ILK siRNA脂质体转染细胞,转染6h后,加入2组培养液处理24h,检测ILK、细胞增生核抗原（PCNA）、LECs转化指标α-SMA和FN在mRNA水平的表达。结果高糖组培养6h和24h,SRA01/04细胞ILK mRNA是正常对照组的2.48倍和2.32倍（P〈0.01）,刺激后24h,SRA01/04细胞PCNA、α-SMA、FN的mRNA表达分别是正常对照组的1.75、1.96和1.75倍（P〈0.01）。ILK siRNA干扰后,正常对照组ILK的表达是非转染细胞的30%,高糖组转染细胞ILK mRNA水平（P〈0.01）是非转染细胞的21%（P〈0.01）,转染细胞PCNA、α-SMA和FN的表达分别是非转染细胞的29%、33%和39%（P〈0.01）。结论高浓度葡萄糖可诱导LECs增生、上皮向间质转化及ILK表达上调,抑制ILK的高表达能阻止这些过程。

英文摘要：

Objective Integrin-linked kinase （ILK） is a serine-threonine kinase. It can be stimulated by high glucose and mainly involved in diabetic complications in kidney. The purpose of this study was to investigate the effects of ILK on cell proliferation and epithelial-to-mesenehymal transition induced by high glucose in human lens epithelial cells（LECs） in vitro. Methods Human LECs line SRA01/04 cells were cultured in DMEM containing 2% serum and exposed to 5.5 mmol/L or 30. 5 mmol/L glucose as control and high glucose group, respectively. The expression of ILK mRNA was analyzed by reverse transcriptase PCR at 0,6,24 hours after treatment of different concentrations of glucose. A small-interfering RNA for ILK gene was selected and the cells were transfected. Six hours after transfection, the cells were exposed to normal or high concentration of glucose for 24 hours. The expression of ILK, proliferating cell nuclear antigen （PCNA） , α-SMA and fihronectin （FN） at mRNA level was detected by RT-PCR to evaluate the cell proliferation and epithelial-to-mesenchymal transition. Results The expression of ILK mRNA in cultured cells of high glucose group increased by 2. 48 and 2.32 folds more than control group at 6 and 24 hours （P 〈 0.01 ）. Level of PCNA mRNA, α-SMA mRNA, and FN mRNA increased by 1.75,1.96 and 1.75 folds in high glucose group compared with normal one at 24 hours（ P 〈 0. 01 ）. After transfected with ILK siRNA ,the expression of ILK mRNA was reduced to 30% of normal control cells. In the transfected cells from high glucose group,ILK expression reduced to 21% of untransfected cells, and that of PCNA, α-SMA, and FN was 29% ,33% and 39% of untransfected cells, respectively （ P 〈 0. 01 ）. Conclusion High glucose stimulates cell proliferation and epithelial-to-mesenehymal transition and upregulates the expression of ILK in human LECs. ILK suppresses cell proliferation and epithelial-to-mesenchymal transition induced by high glucose.