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Biol Pharm Bull ; 42(9): 1491-1499, 2019 Sep 01.
Article in English | MEDLINE | ID: mdl-31204351

ABSTRACT

Endothelial cell injury and apoptosis induced by oxidative stress serve important roles in many vascular diseases. The repair of endothelial cell vascular injury relies on the function of local endothelial progenitor cells (EPCs). Our previous study indicated that epimedin C, a major flavonoid derived from Herba epimedii (yin yang huo), could promote vascularization by inducing endothelial-like differentiation of mesenchymal stem cells C3H/10T1/2 both in vivo and in vitro. In view of the significant cardiovascular protective effects of Herba epimedii, we detected a protective effect of epimedin C on hydrogen peroxide (H2O2)-induced peroxidation injury in human umbilical vein endothelial cells (HUVECs) and the role of EPC in this process. The results show that epimedin C increased the expression of the stem cell marker, CD34 and PROM1, and subsequently enhanced the expression and function of vascular endothelial growth factor and matrix metalloproteinase (MMP)-2 in local vascular endothelial cells. In conclusion, epimedin C protects H2O2-induced peroxidation injury by enhancing the function of endothelial progenitor HUVEC populations.


Subject(s)
Flavonoids/pharmacology , Human Umbilical Vein Endothelial Cells/drug effects , Hydrogen Peroxide/toxicity , Oxidative Stress/drug effects , Protective Agents/pharmacology , Apoptosis/drug effects , Cell Survival/drug effects , Cells, Cultured , Human Umbilical Vein Endothelial Cells/metabolism , Humans , L-Lactate Dehydrogenase/metabolism , Vascular Endothelial Growth Factor A/metabolism
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