Please use this identifier to cite or link to this item: https://doi.org/10.3390/ijms18040844
Title: Hypaphorine attenuates lipopolysaccharide-induced endothelial inflammation via regulation of TLR4 and PPAR-γ dependent on PI3K/Akt/mTOR signal pathway
Authors: Sun, H 
Zhu, X
Cai, W
Qiu, L
Keywords: hypaphorine
indole alkaloid
interleukin 1beta
lipopolysaccharide
monocyte chemotactic protein 1
peroxisome proliferator activated receptor gamma
phosphatidylinositol 3 kinase
protein kinase B
rapamycin
toll like receptor 4
tumor necrosis factor
unclassified drug
vascular cell adhesion molecule 1
autacoid
biological marker
cytokine
indole derivative
lenticin
lipopolysaccharide
peroxisome proliferator activated receptor gamma
phosphatidylinositol 3 kinase
protein binding
protein kinase B
target of rapamycin kinase
toll like receptor 4
Article
cell culture
controlled study
densitometry
enzyme linked immunosorbent assay
human
human cell
immunofluorescence microscopy
inflammation
real time polymerase chain reaction
signal transduction
stimulation
Western blotting
drug effects
enzyme activation
genetics
inflammation
metabolism
pathology
signal transduction
vascular endothelium
Biomarkers
Cytokines
Endothelium, Vascular
Enzyme Activation
Humans
Indoles
Inflammation
Inflammation Mediators
Lipopolysaccharides
Phosphatidylinositol 3-Kinases
PPAR gamma
Protein Binding
Proto-Oncogene Proteins c-akt
Signal Transduction
Toll-Like Receptor 4
TOR Serine-Threonine Kinases
Issue Date: 2017
Publisher: MDPI
Citation: Sun, H, Zhu, X, Cai, W, Qiu, L (2017). Hypaphorine attenuates lipopolysaccharide-induced endothelial inflammation via regulation of TLR4 and PPAR-γ dependent on PI3K/Akt/mTOR signal pathway. International Journal of Molecular Sciences 18 (4) : 844. ScholarBank@NUS Repository. https://doi.org/10.3390/ijms18040844
Rights: Attribution 4.0 International
Abstract: Endothelial lesion response to injurious stimuli is a necessary step for initiating inflammatory cascades in blood vessels. Hypaphorine (Hy) from different marine sources is shown to exhibit anti-inflammatory properties. However, the potential roles and possible molecular mechanisms of Hy in endothelial inflammation have yet to be fully clarified. We showed that Hy significantly inhibited the positive effects of lipopolysaccharide (LPS) on pro-inflammatory cytokines expressions, including tumor necrosis factor-α (TNF-α)), interleukin-1β (IL-1β), monocyte chemoattractant protein 1 (MCP-1) and vascular cellular adhesion molecule-1 (VCAM-1), as well as induction of the phosphorylation of Akt and mTOR in HMEC-1 cells. The downregulated peroxisome proliferator-activated receptor γ (PPAR-γ) and upregulated toll-like receptor 4 (TLR4) expressions in LPS-challenged endothelial cells were prevented by Hy. Inhibition of both PI3K and mTOR reversed LPS-stimulated increases in TLR4 expressions and decreases in PPAR-γ levels. Genetic silencing of TLR4 or PPAR-γ agonist pioglitazone obviously abrogated the levels of pro-inflammatory cytokines in LPS-treated HMEC-1 cells. These results suggest that Hy may exert anti-inflammatory actions through the regulation of TLR4 and PPAR-γ dependent on PI3K/Akt/mTOR signal pathways. Hy may be considered as a therapeutic agent that can potentially relieve or ameliorate endothelial inflammation-associated diseases. © 2017 by the authors. Licensee MDPI, Basel, Switzerland.
Source Title: International Journal of Molecular Sciences
URI: https://scholarbank.nus.edu.sg/handle/10635/183535
ISSN: 1661-6596
DOI: 10.3390/ijms18040844
Rights: Attribution 4.0 International
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