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Antiangiogenic Effect of Ethanol Extract of Vigna angularis via Inhibition of Phosphorylation of VEGFR2, Erk, and Akt.

Kwon OS, Jeong MS, Kim B, Kim SH - Evid Based Complement Alternat Med (2015)

Bottom Line: EVA showed weak cytotoxicity in HUVECs, while it significantly suppressed the VEGF induced proliferation of HUVECs.Of note, EVA effectively attenuated the phosphorylation of VEGFR2, Erk, and Akt in VEGF-treated HUVECs.Overall, our findings suggest that EVA inhibits angiogenesis in VEGF-treated HUVECs via inhibition of phosphorylation of VEGFR2, ERK, and Akt.

View Article: PubMed Central - PubMed

Affiliation: Department of East West Medical Science, Graduate School of East West Medical Science, Kyung Hee University, Suwon 446-701, Republic of Korea.

ABSTRACT
Though dietary azuki bean (Vigna angularis) seed containing antioxidant proanthocyanidins was known to have multibiological activities including antioxidant, hypotensive, anti-inflammatory, and immunomodulatory activities, the antiangiogenic activity of ethanol extract of Vigna angularis (EVA) was never reported so far. In the present study, the antiangiogenic mechanism of EVA was examined in human umbilical vein endothelial cells (HUVECs). EVA showed weak cytotoxicity in HUVECs, while it significantly suppressed the VEGF induced proliferation of HUVECs. Consistently, wound healing assay revealed that EVA inhibited the VEGF induced migration of HUVECs. Also, EVA abrogated the VEGF induced tube formation of HUVECs in a concentration dependent fashion. Furthermore, Matrigel plug assay showed that EVA significantly reduced the hemoglobin level of Matrigel plug in mice compared to untreated control. Of note, EVA effectively attenuated the phosphorylation of VEGFR2, Erk, and Akt in VEGF-treated HUVECs. Overall, our findings suggest that EVA inhibits angiogenesis in VEGF-treated HUVECs via inhibition of phosphorylation of VEGFR2, ERK, and Akt.

No MeSH data available.


Related in: MedlinePlus

EVA inhibits VEGF induced proliferation in HUVECs. Cell proliferation was determined using a BrdU colorimetric assay kit. Cells (5 × 103 cells/well) were seeded onto 96-well plates and incubated for 24 h. After 6 h starvation, the cells were exposed to various concentrations of EVA (10, 20, and 30 μg/mL) in the presence or absence of VEGF (50 ng/mL) and incubated for 48 h at 37°C. Data are presented as means ± SD. ∗, #p < 0.05 versus VEGF only treated group.
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fig2: EVA inhibits VEGF induced proliferation in HUVECs. Cell proliferation was determined using a BrdU colorimetric assay kit. Cells (5 × 103 cells/well) were seeded onto 96-well plates and incubated for 24 h. After 6 h starvation, the cells were exposed to various concentrations of EVA (10, 20, and 30 μg/mL) in the presence or absence of VEGF (50 ng/mL) and incubated for 48 h at 37°C. Data are presented as means ± SD. ∗, #p < 0.05 versus VEGF only treated group.

Mentions: Cytotoxicity of EVA was evaluated in HUVECs using MTT assay. As shown in Figure 1, EVA decreased the viability of HUVECs to ~60% at the concentration of 50 µM for 48 h. EVA treatment showed cytotoxicity in VEGF-treated HUVECs in a concentration dependent manner (Figure 2).


Antiangiogenic Effect of Ethanol Extract of Vigna angularis via Inhibition of Phosphorylation of VEGFR2, Erk, and Akt.

Kwon OS, Jeong MS, Kim B, Kim SH - Evid Based Complement Alternat Med (2015)

EVA inhibits VEGF induced proliferation in HUVECs. Cell proliferation was determined using a BrdU colorimetric assay kit. Cells (5 × 103 cells/well) were seeded onto 96-well plates and incubated for 24 h. After 6 h starvation, the cells were exposed to various concentrations of EVA (10, 20, and 30 μg/mL) in the presence or absence of VEGF (50 ng/mL) and incubated for 48 h at 37°C. Data are presented as means ± SD. ∗, #p < 0.05 versus VEGF only treated group.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4556864&req=5

fig2: EVA inhibits VEGF induced proliferation in HUVECs. Cell proliferation was determined using a BrdU colorimetric assay kit. Cells (5 × 103 cells/well) were seeded onto 96-well plates and incubated for 24 h. After 6 h starvation, the cells were exposed to various concentrations of EVA (10, 20, and 30 μg/mL) in the presence or absence of VEGF (50 ng/mL) and incubated for 48 h at 37°C. Data are presented as means ± SD. ∗, #p < 0.05 versus VEGF only treated group.
Mentions: Cytotoxicity of EVA was evaluated in HUVECs using MTT assay. As shown in Figure 1, EVA decreased the viability of HUVECs to ~60% at the concentration of 50 µM for 48 h. EVA treatment showed cytotoxicity in VEGF-treated HUVECs in a concentration dependent manner (Figure 2).

Bottom Line: EVA showed weak cytotoxicity in HUVECs, while it significantly suppressed the VEGF induced proliferation of HUVECs.Of note, EVA effectively attenuated the phosphorylation of VEGFR2, Erk, and Akt in VEGF-treated HUVECs.Overall, our findings suggest that EVA inhibits angiogenesis in VEGF-treated HUVECs via inhibition of phosphorylation of VEGFR2, ERK, and Akt.

View Article: PubMed Central - PubMed

Affiliation: Department of East West Medical Science, Graduate School of East West Medical Science, Kyung Hee University, Suwon 446-701, Republic of Korea.

ABSTRACT
Though dietary azuki bean (Vigna angularis) seed containing antioxidant proanthocyanidins was known to have multibiological activities including antioxidant, hypotensive, anti-inflammatory, and immunomodulatory activities, the antiangiogenic activity of ethanol extract of Vigna angularis (EVA) was never reported so far. In the present study, the antiangiogenic mechanism of EVA was examined in human umbilical vein endothelial cells (HUVECs). EVA showed weak cytotoxicity in HUVECs, while it significantly suppressed the VEGF induced proliferation of HUVECs. Consistently, wound healing assay revealed that EVA inhibited the VEGF induced migration of HUVECs. Also, EVA abrogated the VEGF induced tube formation of HUVECs in a concentration dependent fashion. Furthermore, Matrigel plug assay showed that EVA significantly reduced the hemoglobin level of Matrigel plug in mice compared to untreated control. Of note, EVA effectively attenuated the phosphorylation of VEGFR2, Erk, and Akt in VEGF-treated HUVECs. Overall, our findings suggest that EVA inhibits angiogenesis in VEGF-treated HUVECs via inhibition of phosphorylation of VEGFR2, ERK, and Akt.

No MeSH data available.


Related in: MedlinePlus