FOLLOWUS
1. Fujian Academy of Integrative Medicine,Fuzhou,China
2. Fujian Key Laboratory of Integrative Medicine on Geriatrics, Fujian University of Traditional Chinese Medicine,Fuzhou,China
纸质出版日期:2015,
网络出版日期:2015-3-17,
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Zhao, Jy., Lin, W., Zhuang, Qc. et al. Bear bile powder inhibits angiogenesis in vivo and in vitro, ., Chin. J. Integr. Med. 21, 369–375 (2015). https://doi.org/10.1007/s11655-015-2062-0
Jin-yan Zhao, Wei Lin, Qun-chuan Zhuang, et al. Bear bile powder inhibits angiogenesis in vivo and in vitro[J]. Chinese Journal of Integrative Medicine, 2015,21(5):369-375.
Zhao, Jy., Lin, W., Zhuang, Qc. et al. Bear bile powder inhibits angiogenesis in vivo and in vitro, ., Chin. J. Integr. Med. 21, 369–375 (2015). https://doi.org/10.1007/s11655-015-2062-0 DOI:
Jin-yan Zhao, Wei Lin, Qun-chuan Zhuang, et al. Bear bile powder inhibits angiogenesis in vivo and in vitro[J]. Chinese Journal of Integrative Medicine, 2015,21(5):369-375. DOI: 10.1007/s11655-015-2062-0.
To evaluate the effect of bear bile powder (BBP) on angiogenesis
and investigate the underlying molecular mechanisms. A chick embryo chorioallantoic membrane (CAM) assay was used to evaluate the angiogensis in vivo. Human umbilical vein endothelial cells (HUVECs) were treated with 0
0.25
0.5
0.75
and 1.0 mg/mL of BBP for 24
48 and 72 h
respectively. The 3-(4
5-dimethylthiazol-2-yl)-2
5-diphenyltetrazolium bromide assay was performed to determine the viability of HUVECs. Cell cycle progression of HUVECs was examined by fluorescence-activated cell sorting (FACS) analysis with propidium iodide staining. HUVEC migration was determined by wound healing method. An ECMatrix gel system was used to evaluate the tube formation of HUVECs. The mRNA and protein expression of vascular endothelial growth factor (VEGF)-A in both HUVECs and HepG2 human cells were examined by reverse transcription-polymerase chain reaction and enzyme linked immunosorbent assay
respectively. Compared with the untreated group
BBP inhibited angiogenesis in vivo in the CAM model (P< 0.01). In addition
treatment with 0.25–1 mg/mL of BBP for 24
48
or 72 h respectively reduced cell viability by 14%–27%
29%–69% and 33%–91%
compared with the untreated control cells (P< 0.01). Additionally
BBP inhibited the proliferation of HUVECs via blocking the cell cycle G to S progression
compared with the S phase of untreated cells 48.05%± 5.00%
0.25–0.75 mg/mL BBP reduced S phase to 40.38%± 5.30%
36.54± 4.50% and 32.13± 3.50%
respectively (Pglt; 0.05). Moreover
BBP inhibited the migration and tube formation of HUVECs
compared with the tube length of untreated cells 100%± 12%
0.25–0.75 mg/mL BBP reduced the tube length to 62%± 9%
43%± 5% and 17%± 3%
respectively (p< 0.01). Furthermore
BBP treatment down-regulated the mRNA and protein expression levels of VEGF-A in both HepG2 cells and HUVECs. BBP could inhibit the angiogenesis by reducing VEGF-A expression
which may
in part
explain its anti-tumor activity.
To evaluate the effect of bear bile powder (BBP) on angiogenesis
and investigate the underlying molecular mechanisms. A chick embryo chorioallantoic membrane (CAM) assay was used to evaluate the angiogensis in vivo. Human umbilical vein endothelial cells (HUVECs) were treated with 0
0.25
0.5
0.75
and 1.0 mg/mL of BBP for 24
48 and 72 h
respectively. The 3-(4
5-dimethylthiazol-2-yl)-2
5-diphenyltetrazolium bromide assay was performed to determine the viability of HUVECs. Cell cycle progression of HUVECs was examined by fluorescence-activated cell sorting (FACS) analysis with propidium iodide staining. HUVEC migration was determined by wound healing method. An ECMatrix gel system was used to evaluate the tube formation of HUVECs. The mRNA and protein expression of vascular endothelial growth factor (VEGF)-A in both HUVECs and HepG2 human cells were examined by reverse transcription-polymerase chain reaction and enzyme linked immunosorbent assay
respectively. Compared with the untreated group
BBP inhibited angiogenesis in vivo in the CAM model (P< 0.01). In addition
treatment with 0.25–1 mg/mL of BBP for 24
48
or 72 h respectively reduced cell viability by 14%–27%
29%–69% and 33%–91%
compared with the untreated control cells (P< 0.01). Additionally
BBP inhibited the proliferation of HUVECs via blocking the cell cycle G to S progression
compared with the S phase of untreated cells 48.05%± 5.00%
0.25–0.75 mg/mL BBP reduced S phase to 40.38%± 5.30%
36.54± 4.50% and 32.13± 3.50%
respectively (Pglt; 0.05). Moreover
BBP inhibited the migration and tube formation of HUVECs
compared with the tube length of untreated cells 100%± 12%
0.25–0.75 mg/mL BBP reduced the tube length to 62%± 9%
43%± 5% and 17%± 3%
respectively (p< 0.01). Furthermore
BBP treatment down-regulated the mRNA and protein expression levels of VEGF-A in both HepG2 cells and HUVECs. BBP could inhibit the angiogenesis by reducing VEGF-A expression
which may
in part
explain its anti-tumor activity.
bear bile powderhepatocellular carcinomatumor angiogenesishuman umbilical vein endothelial cellsChinese Medicine
bear bile powderhepatocellular carcinomatumor angiogenesishuman umbilical vein endothelial cellsChinese Medicine
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