PUBLICATION
Diphlorethohydroxycarmalol Isolated from Ishige okamurae Represses High Glucose-Induced Angiogenesis In Vitro and In Vivo.
- Authors
- Fernando, K.H.N., Yang, H.W., Jiang, Y., Jeon, Y.J., Ryu, B.
- ID
- ZDB-PUB-181013-2
- Date
- 2018
- Source
- Marine drugs 16(10): (Journal)
- Registered Authors
- Jeon, You-Jin
- Keywords
- EA.hy926, Ishige okamurae, VEGFR-2, angiogenesis, diabetes, diphlorethohydroxycarmalol, zebrafish
- MeSH Terms
-
- Angiogenesis Inhibitors/pharmacology*
- Animals
- Cell Line
- Cell Movement/drug effects
- Cell Proliferation/drug effects
- Embryo, Nonmammalian/drug effects
- Embryo, Nonmammalian/metabolism
- Endothelial Cells/drug effects
- Endothelial Cells/metabolism
- Glucose/adverse effects*
- Heterocyclic Compounds, 3-Ring/pharmacology*
- Humans
- Hypoglycemic Agents/pharmacology
- Phaeophyceae/chemistry*
- Signal Transduction/drug effects
- Vascular Endothelial Growth Factor A/metabolism
- Zebrafish
- PubMed
- 30308943 Full text @ Mar. Drugs
Citation
Fernando, K.H.N., Yang, H.W., Jiang, Y., Jeon, Y.J., Ryu, B. (2018) Diphlorethohydroxycarmalol Isolated from Ishige okamurae Represses High Glucose-Induced Angiogenesis In Vitro and In Vivo.. Marine drugs. 16(10).
Abstract
Diabetes mellitus causes abnormalities of angiogenesis leading to vascular dysfunction and serious pathologies. Diphlorethohydroxycarmalol (DPHC), which is isolated from Ishige okamurae, is well known for its bioactivities, including antihyperglycemic and protective functions against diabetes-related pathologies. In the present study, the inhibitory effect of DPHC on high glucose-induced angiogenesis was investigated on the human vascular endothelial cell line EA.hy926. DPHC inhibited the cell proliferation, cell migration, and tube formation in cells exposed to 30 mM of glucose to induce angiogenesis. Furthermore, the effect of DPHC against high glucose-induced angiogenesis was evaluated in zebrafish embryos. The treatment of embryos with DPHC suppressed high glucose-induced dilation in the retinal vessel diameter and vessel formation. Moreover, DPHC could inhibit high glucose-induced vascular endothelial growth factor receptor 2 (VEGFR-2) expression and its downstream signaling cascade. Overall, these findings suggest that DPHC is actively involved in the suppression of high glucose-induced angiogenesis. Hence, DPHC is a potential agent for the development of therapeutics against angiogenesis induced by diabetes.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping