目的　探讨血管内皮生长因子（VEGF）对转化生长因子β1（TGF-β1）诱导的肾小管上皮间充质转化（EMT）的作用，及其与结缔组织生长因子（CTGF）、PI3K-Akt信号通路的关系。 方法 （1）将体外培养的HK2细胞分为正常对照组、TGF-β1（5 μg/L，下同）组、VEGF组（100 μg/L，下同）、TGF-β1＋VEGF组。HK2细胞体外培养48 h，用免疫组化双染方法检测肾小管上皮细胞α平滑肌肌动蛋白（α-SMA）和E钙黏蛋白的表达。（2）将体外培养的HK2细胞分为正常对照组、TGF-β1组、VEGF组、TGF-β1＋VEGF组、PI3K-Akt信号通路阻断剂LY294002组（25 μmol/L，下同）、TGF-β1＋LY294002组、VEGF＋LY294002组、TGF-β1＋VEGF＋LY294002组。HK2细胞体外培养48 h，用Western印迹和RT-PCR方法检测α-SMA和CTGF的表达；用ELISA方法检测培养上清中纤连蛋白（FN）和I型胶原（ColⅠ）的表达。 结果 免疫组化结果显示，TGF-β1组α-SMA表达比正常对照组增强，而E钙黏蛋白表达减弱； TGF-β1＋VEGF组α-SMA表达比TGF-β1组显著减弱，而E钙黏蛋白表达增强。 TGF-β1组α-SMA、CTGF蛋白和 mRNA及FN、ColⅠ表达比正常对照组显著增强（均P < 0.05）；TGF-β1＋VEGF组α-SMA、CTGF蛋白和mRNA及FN、ColⅠ表达比TGF-β1组显著减弱（均P < 0.05）；TGF-β1＋VEGF＋LY294002组α-SMA、CTGF蛋白和 mRNA及FN、ColⅠ表达比TGF-β1＋VEGF组显著增强（均P < 0.05）。 结论　VEGF能抑制TGF-β1诱导的体外培养的HK2细胞发生EMT，其机制可能与VEGF下调HK2细胞CTGF表达及减少细胞外FN、ColⅠ合成有关。VEGF的这种作用可能部分通过PI3K-Akt信号转导通路实现，其确切机制有待进一步研究。

Objective To examine the relationship of the inhibitory effect of vascular endothelial growth factor(VEGF) on epithelial-mesenchymal transition (EMT) induced by TGF-β1 in HK2 cells with the expression of connective tissue growth factor (CTGF) and PI3K-Akt pathway. Methods The cultured HK2 cells were divided into the following groups: normal control group, TGF-β1(5 μg/L) group, VEGF (100 μg/L) group, TGF-β1 plus VEGF group. LY294002 (25 μmol/L), the blocker of PI3K-Akt pathway, was added to each of above-mentioned groups for the second part of the study. α-smooth muscle actin (α-SMA) and E-cadherin expressions of HK2 cells were assessed with double-stain immunocytochemistry method. The mRNA and protein expressions of α-SMA and CTGF of cells were assessed with RT-PCR and Western blot. The expressions of fibronectin(FN) and collagen I (ColⅠ) in medium were assessed with ELISA. Results The expressions of α-SMA and CTGF significantly increased in HK2 cells treated with TGF-β1 compared with those in normal control（P<0.05）, while significantly decreased in cells co-treated with TGF-β1 and VEGF compared with those treated with TGF-β1 alone (P<0.05, respectively). The expression of E-cadherin was exactly opposite to that of α-SMA. When LY294002 was added to TGF-β1 and VEGF co-treated cells, the expressions of α-SMA, CTGF, FN and ColⅠ were markedly up-regulated, when compared with those without LY294002 treatment(P<0.05). Conclusion Inhibitory effect of VEGF on TGF-β1-induced EMT of HK2 cells in vitro may be related to down-regulation of CTGF expression and reduction of FN and ColⅠ, which may be partly dependent on PI3K-Akt pathway.