PUBLICATION
Ardisia crispa root hexane fraction suppressed angiogenesis in human umbilical vein endothelial cells (HUVECs) and in vivo zebrafish embryo model
- Authors
- Wen Jun, L., Pit Foong, C., Abd Hamid, R.
- ID
- ZDB-PUB-190924-10
- Date
- 2019
- Source
- Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 118: 109221 (Journal)
- Registered Authors
- Keywords
- Angiogenesis inhibitor, Ardisia crispa, Cell migration assay, HUVECs, VEGF
- MeSH Terms
-
- Animals
- Apoptosis
- Ardisia/chemistry*
- Cell Cycle Checkpoints
- Cell Differentiation
- Cell Movement
- Cell Proliferation
- Embryo, Nonmammalian/metabolism*
- Hexanes/chemistry*
- Human Umbilical Vein Endothelial Cells/metabolism*
- Human Umbilical Vein Endothelial Cells/pathology
- Humans
- Matrix Metalloproteinases/metabolism
- Models, Animal
- Neovascularization, Pathologic/drug therapy*
- Neovascularization, Pathologic/pathology
- Plant Roots/chemistry*
- Zebrafish/embryology*
- PubMed
- 31545225 Full text @ Biomed. Pharmacother.
Citation
Wen Jun, L., Pit Foong, C., Abd Hamid, R. (2019) Ardisia crispa root hexane fraction suppressed angiogenesis in human umbilical vein endothelial cells (HUVECs) and in vivo zebrafish embryo model. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 118:109221.
Abstract
Ardisia crispa Thunb. A. DC. (Primulaceae) has been used extensively as folk-lore medicine in South East Asia including China and Japan to treat various inflammatory related diseases. Ardisia crispa root hexane fraction (ACRH) has been thoroughly studied by our group and it has been shown to exhibit anti-inflammatory, anti-hyperalgesic, anti-arthritic, anti-ulcer, chemoprevention and suppression against inflammation-induced angiogenesis in various animal model. Nevertheless, its effect against human endothelial cells in vitro has not been reported yet. Hence, the aim of the study is to investigate the potential antiangiogenic property of ACRH in human umbilical vein endothelial cells (HUVECs) and zebrafish embryo model. ACRH was separated from the crude ethanolic extract of the plant's root in prior to experimental studies. MTT assay revealed that ACRH exerted a concentration-dependent antiproliferative effect on HUVEC with the IC50 of 2.49 ± 0.04 μg/mL. At higher concentration (10 μg/mL), apoptosis was induced without affecting the cell cycle distribution. Angiogenic properties including migration, invasion and differentiation of HUVECs, evaluated via wound healing, trans-well invasion and tube formation assay respectively, were significantly suppressed by ACRH in a concentration-dependent manner. Noteworthily, significant antiangiogenic effects were observed even at the lowest concentration used (0.1 μg/mL). Expression of proMMP-2, vascular endothelial growth factor (VEGF)-C, VEGF-D, Angiopoietin-2, fibroblast growth factor (FGF)-1, FGF-2, Follistatin, and hepatocyte growth factor (HGF) were significantly reduced in various degrees by ACRH. The ISV formation in zebrafish embryo was significantly suppressed by ACRH at the concentration of 5 μg/mL. These findings revealed the potential of ACRH as antiangiogenic agent by suppressing multiple proangiogenic proteins. Thus, it can be further verified via the transcription of these proteins from their respective DNA, in elucidating their exact pathways.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping