目的    观察肾损伤分子1（KIM-1）对高糖诱导大鼠肾小管上皮细胞单核细胞趋化蛋白1（MCP-1）和纤维连接蛋白（FN）表达的影响，探讨KIM-1参与糖尿病肾病肾间质纤维化（RIF）的可能机制。 方法    体外培养大鼠肾小管上皮细胞（NRK52E）并分为5组：⑴ 空白对照组（D-葡萄糖5.6 mmol/L）；⑵ 高渗组（D-葡萄糖 5.6 mmol/L＋D-甘露醇 24.4 mmol/L）；⑶ 高糖组（D-葡萄糖30 mmol/L）；⑷ siRNA对照组；⑸ KIM-1 siRNA组。ELISA法检测细胞上清液中MCP-1和FN蛋白水平；Western 印迹法检测细胞KIM-1蛋白的表达；RT-PCR法检测细胞KIM-1、MCP-1、FN mRNA的表达。 结果    与空白对照组相比，高糖组细胞KIM-1蛋白和mRNA的表达于12 h时间点增高（P＜0.05），48 h时达最高值（P＜0.05）；MCP-1及FN蛋白和mRNA的表达于24 h时增多（P＜0.05），48 h时达最高值（P＜0.05）。与高糖组相比，KIM-1 siRNA转染组MCP-1及FN蛋白和mRNA表达显著减少（均P＜0.05）。 结论    下调KIM-1的表达能显著抑制高糖条件下肾小管上皮细胞表达MCP-1和FN，提示KIM-1可能通过调控MCP-1及FN的表达参与糖尿病肾病肾间质纤维化（RIF）的进程。  

Objective    To evaluate the effects of KIM-1 on high glucose induced the expression of MCP-1 and FN in rat tubular epithelial cells and to explore the possible mechanisms of KIM-1 involved in renal interstitial fibrosis of DN.    Methods    The rat renal tubular epithelial cells (NRK52E) were cultured in vitro and divided into five groups: Normal control group (D-glucose 5.6 mmol/L), Hypertonic group (D-glucose 5.6 mmol/L＋D-mannitol 24.4 mmol/L), High glucose group (D-glucose 30 mmol/L), Control siRNA group，KIM-1 siRNA group. ELISA assay was used to assess the levels of MCP-1 and FN in the cells supernatant; Western blotting was used to detect the protein expression of KIM-1; RT-PCR was used to detect mRNA expression of KIM-1, MCP-1 and FN.    Results    Compared with the control group, the protein and mRNA expression of KIM-1 in the high glucose group were increased at 12 h (P＜0.05), and reached the peak at 48 h (P＜0.05); the protein and mRNA expression of MCP-1 and FN in high glucose group were increased at 24 h significantly (P＜0.05), and peaked at 48 h (P＜0.05). Compared with the high glucose group, the protein and mRNA expressions of MCP-1 and FN in KIM-1 siRNA group were decreased (P＜0.05).    Conclusions    Down-regulating the expression of KIM-1 can significantly inhibit the expression of MCP-1 and FN, which suggests that KIM-1 may be involved in renal interstitial fibrosis of DN by regulating expression of MCP-1 and FN.