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目的 :观察高糖条件下制备的视网膜 Müller细胞条件培养基 (HGMCM)及抗 VEGF对血管内皮细胞的作用。方法 :采用免疫荧光、流式细胞术和 Boyden小室迁移实验观察 HGMCM,含 wortmannin及含 VEGF单克隆抗体 HGMCM对血管内皮细胞的作用。结果 :HGMCM可促进体外培养的血管内皮细胞的增殖和迁移(14 2 .0 0± 15 .32 /视野 ) ,wortm annin、VEGF单克隆抗体可明显抑制 HGMCM诱导的血管内皮细胞的增殖和迁移(89.0 0± 9.2 8/视野 ,93.0 0± 9.6 4 /视野 ) ,使血管内皮细胞被阻滞于 G1 / S转变期 ,含 wortm ennin和 VEGF单克隆抗体 HGMCM组与 HGMCM组比较 ,差异均有显著性 (P<0 .0 1)。结论 :HGMCM诱导血管内皮细胞的增殖和迁移一部分是通过 VEGF发挥作用的 ,拮抗 VEGF的活性可抑制血管内皮细胞的增殖和迁移 ,进而抑制新生血管形成。
OBJECTIVE: To observe the effects of HGMCM (retinal Müller cells conditioned medium) and anti-VEGF on vascular endothelial cells (HUVECs) cultured in high glucose. Methods: The effects of HGMCM, wortmannin and VEGF-containing monoclonal antibody HGMCM on vascular endothelial cells were observed by immunofluorescence, flow cytometry and Boyden chamber migration assay. Results: HGMCM could promote the proliferation and migration of vascular endothelial cells cultured in vitro (14 2.000 ± 15.32 / field of view). The monoclonal antibody of wortm annin and VEGF could significantly inhibit the proliferation and migration of HGMCM-induced vascular endothelial cells 89.0 ± 9.28 / field of vision, 93.0 ± 9.64 / field of vision), vascular endothelial cells were arrested in the G1 / S transition phase, containing wortm ennin and VEGF monoclonal antibody HGMCM group compared with the HGMCM group, the difference was significant Sex (P <0. 01). CONCLUSION: HGMCM induces proliferation and migration of vascular endothelial cells in part through the action of VEGF. Antagonizing the activity of VEGF can inhibit the proliferation and migration of vascular endothelial cells, and then inhibit the formation of neovascularization.