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Effects of Fuantai-03 Isolated from Dasyatis akajei on the Apoptosis of Human Umbilical Vein Endothelial Cells and Mouse Wound Healing
Su Weiming1, Huang Laizhen1, Ma Rundi1*, Yu Lijian1*, Wang Qiang1, Zhang Xiaoyu1,2, Yu Tingxi1,3*
1Key Laboratory of Marine Materia Medica, Guangdong Ocean University, Zhanjiang 524025, China; 2Department of Otorhinolaryngology-Head and Neck Surgery, University of Maryland School of Medicine, MD 21228; 3Cell Biology Gr
Abstract: The present study was undertaken to investigate the effects of Fuantai-03 (FAT-03) isolated from Dasyatis akajei effected on the apoptosis of human umbilical vein endothelial cells and wound healing. MTT assay was performed to measure the effect of FAT-03 on cell growth; migration assay was performed using a Transwell model with polycarbonate membrane; apoptotic induction was determined by fluorescence microscopy and flow cytometry; Western blot analysis was performed for examing expressions of vascular endothelial growth factor (VEGF)， Bcl-2 and Bax. Mouse wound model was applied to investigate the effect of FAT-03 on wound healing; immunohistochemical staining assay was adopted to examine the microvessel density (MVD) and expression of VEGF in wound tissues. FAT-03 obviously inhibited proliferation and migration of HUVECs in a dose- and timedependent manner the values of IC50 for the effect of FAT-03 on HUVECs at 24， 48， 72 h are 0.22 mg/mL， 0.17 mg/mL， 0.09 mg/mL， respectively， but FAT-03 did not show significant effect on the growth of human nasopharyngeal carcinoma cell line (CNE-2Z). 0.16 mg/mL FAT-03 decreased the percentage of migrating HUVECs at 24 h by 57.9% (P<0.01). FAT-03-treated HUVECs showed typical morphologic and cellular evidences of apoptosis. The expressions of VEGF and Bcl-2 in the FAT-03-treated HUVECs were evidently down-regulated， and the expression of Bax was obviously up-regulated. FAT-03 markedly decreased the MVD (P<0.05) and down-regulated the expression of VEGF in mouse wound tissues， and inhibited tissue repairing. These findings provide evidences that FAT-03 significantly inhibits the proliferation and migration of HUVECs and induces their apoptosis， and inhibits tissue repairing in mouse wound model. The effects of FAT-03 might result from the down-regulation of expressions of VEGF and Bcl-2 and up-regulation of expression of Bax.
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