目的：研究人非小细胞肺癌A549细胞自分泌VEGF对膜结合补体调节蛋白(membranebounal complement regulatory proteins, mCRPs)的调控及其机制。方法: RTPCR法检测CD46、CD55、CD59、VEGF及其受体(KDR和FLT1)和 IL8及其受体(CXCR1 CXCR2) mRNA在人非小细胞肺癌A549细胞的表达。MTT法检测抗VEGF抗体和抗IL8抗体对A549细胞增殖的影响，流式细胞术检测抗VEGF抗体和抗IL8抗体对A549细胞mCRPs表达水平的影响，Western blotting检测抗VEGF抗体对转录因子KLF2和磷酸化NFκB p65蛋白表达的影响。结果：A549细胞表达膜结合型CD46、CD55和CD59 mRNA，亦表达VEGF及其受体（KDR和FLT1）和 IL8及其受体（CXCR1和CXCR2） mRNA。抗VEGF抗体明显抑制A549细胞的增殖（P<0.05）。终质量浓度0.1 μg/ml抗VEGF抗体封闭72 h，CD55和CD59 mRNA表达下降，膜结合的CD55和CD59蛋白分子表达降低(均P<0.05)；胞质和核KLF2蛋白相对定量值分别从063和0.88下降至0.42和0.66，胞质和胞核磷酸化NFκB p65蛋白相对定量值分别从0.44和0.28下降至0.37和019。结论：A549细胞可能通过自分泌VEGF增加NFκB p65和KLF2转录因子水平，从而上调CD55和CD59的表达。

Objective: To explore the regulatory effect of autocrined VEGF on membranebound complement regulatory proteins (mCRPs) expression in lung cancer A549 cells and the involved mechanisms. Methods: mRNA expressions of CD46, CD55,CD59, VEGF and their receptors (KDR and FLT1), and IL8 and its receptors (CXCR1 CXCR2) in A549 cells were detected by RTPCR. The effects of antiVEGF antibody and antiIL8 antibody on the proliferation and mCRPs expression in A549 cells were examined by MTT assay and flow cytometry, respectively. The effects of antiVEGF antibody on the expression of transcription factor KLF2 and phosphoNFκB p65 were examined by Western blotting analysis. Results: In addition to membrane CD46, CD55 and CD59 mRNA, both VEGF, IL8 and their receptors (KDR, FLT1; CXCR1, CXCR2) mRNA were expressed in A549 cells. AntiVEGF antibody significantly inhibited the proliferation of A549 cells (P<0.05). CD55 and CD59 mRNA and protein levels in A549 cells were decreased after treatment with 0.1 μg/ml antiVEGF antibody for 72 h (P<0.05). The relative values of KLF2 in cytoplasm and nuclear decreased from 0.63 and 0.88 to 0.42 and 0.66 after treatment with antiVEGF antibody, while those of phosphoNFκB p65 decreased from 0.44 and 0.28 to 0.32 and 019. Conclusion: VEGF may enhance CD55 and CD59 expressions in A549 cells through upregulating expressions of NFκB P65 and KLF2 transcription factors in an autocrine manner.

山东省自然科学基金资助项目（No. Y2007C154）