Key result
Ginsenoside-Rg1 stimulated hypoxia-inducible factor-1α accumulation and promoted angiogenesis in human umbilical vein endothelial cells via the PI3K/Akt and p70 S6K pathways under normal oxygen conditions.
Why the study?
Does Ginsenoside-Rg1 promote angiogenesis via HIF-1α upregulation in human umbilical vein endothelial cells?
Population
Human umbilical vein endothelial cells (HUVECs) (fifth to eighth passages)
Comparison
Ginsenoside-Rg1 (150 nM) vs Untreated control
Design
Preclinical
Authors
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Hypothesis-generating for ginsenoside-Rg1 in normoxic angiogenesis; leaves open clinical translation pending in vivo studies.
Does Ginsenoside-Rg1 promote angiogenesis via HIF-1α upregulation in human umbilical vein endothelial cells?
p-value: p=<0.05
Ginsenoside-Rg1 promotes angiogenesis through a hypoxia-independent, PI3K/Akt/p70S6K-mediated upregulation of HIF-1α protein synthesis.
Leung et al. (2011) studied Angiogenesis (in vitro). Ginsenoside-Rg1 vs. Untreated control was evaluated on HIF-1α protein accumulation and angiogenic tube formation (p=<0.05). Ginsenoside-Rg1 stimulated hypoxia-inducible factor-1α accumulation and promoted angiogenesis in human umbilical vein endothelial cells via the PI3K/Akt and p70 S6K pathways under normal oxygen conditions.
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