Bibenzyl from Dendrobium inhibits angiogenesis and its underlying mechanism.
- Author:
Chen-Yuan GONG
1
;
Bin LU
;
Li YANG
;
Lei WANG
;
Li-Li JI
Author Information
1. The MOE Key Laboratory for Standardization of Chinese Medicines, SATCM Key Laboratory for New Resources and Quality Evaluation of Chinese Medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201210, China.
- Publication Type:Journal Article
- MeSH:
Angiogenesis Inhibitors;
administration & dosage;
isolation & purification;
pharmacology;
Animals;
Benzyl Compounds;
administration & dosage;
isolation & purification;
pharmacology;
Bibenzyls;
isolation & purification;
pharmacology;
Cell Count;
Cells, Cultured;
Dendrobium;
chemistry;
Dose-Response Relationship, Drug;
Human Umbilical Vein Endothelial Cells;
Humans;
MAP Kinase Kinase 1;
metabolism;
MAP Kinase Kinase 2;
metabolism;
MAP Kinase Signaling System;
drug effects;
Mice;
Mice, Inbred C57BL;
Neovascularization, Physiologic;
drug effects;
Phosphorylation;
drug effects;
Plants, Medicinal;
chemistry;
Proto-Oncogene Proteins c-raf;
metabolism;
Signal Transduction;
drug effects;
Vascular Endothelial Growth Factor Receptor-2;
metabolism
- From:
Acta Pharmaceutica Sinica
2013;48(3):337-342
- CountryChina
- Language:Chinese
-
Abstract:
Bibenzyl is a type of active compounds abundant in Dendrobium. In the present study, we investigated the inhibitory effects of six bibenzyls isolated from Dendrobium species on vascular endothelial growth factor (VEGF)-induced tube formation in human umbilical vascular endothelial cells (HUVECs). All those bibenzyls inhibited VEGF-induced tube formation at 10 micromol x L(-1) except tristin, and of which moscatilin was found to have the strongest activity at the same concentration. The lowest effective concentration of moscatilin was 1 micromol x L(-1). Further results showed that moscatilin inhibited VEGF-induced capillary-like tube formation on HUVECs in a concentration-dependent manner. Western blotting results showed that moscatilin also inhibited VEGF-induced phosphorylation of VEGFR2 (Flk-1/KDR) and extracellular signal-regulated kinase 1/2 (ERK1/2). Further results showed that moscatilin inhibited VEGF-induced activation of c-Raf and MEK1/2, which are both upstream signals of ERK1/2. Taken together, results presented here demonstrated that moscatilin inhibited angiogenesis via blocking the activation of VEGFR2 (Flk-1/KDR) and c-Raf-MEK1/2-ERK1/2 signals.
