TY - JOUR
T1 - Barrier protective activities of phloroglucinol on lipopolysaccharide (LPS)-induced barrier disruption in human endothelial cells
AU - Bae, Jong Sup
PY - 2012/6
Y1 - 2012/6
N2 - Phloroglucinol plays an important role in oxidative stress, inflammatory responses, and matrix metalloproteinase (MMP) regulation. However, the barrier protective functions of phloroglucinol are not well studied. The objective of this study was to fill this gap. We did this by investigating the barrier protective activities of phloroglucinol on lipopolysaccharide (LPS)-induced barrier disruption in human endothelial cells measured by cellular permeability, monocytes adhesion, and migration toward human endothelial cells. The results showed that phloroglucinol inhibited LPS-induced barrier hyperpermeability, monocyte adhesion, and migration. These inhibitory effects were significantly correlated with the inhibitory functions of phloroglucinol on LPS-induced cell adhesion molecules. Furthermore, LPS-induced nuclear factor-κB (NF-κB) and tumor necrosis factor-κB (TNF-κB) release from human umbilical vein endothelial cells (HUVECs) was inhibited by phloroglucinol. Given these results, phloroglucinol could be a candidate as a therapeutic agent for various systemic inflammatory diseases.
AB - Phloroglucinol plays an important role in oxidative stress, inflammatory responses, and matrix metalloproteinase (MMP) regulation. However, the barrier protective functions of phloroglucinol are not well studied. The objective of this study was to fill this gap. We did this by investigating the barrier protective activities of phloroglucinol on lipopolysaccharide (LPS)-induced barrier disruption in human endothelial cells measured by cellular permeability, monocytes adhesion, and migration toward human endothelial cells. The results showed that phloroglucinol inhibited LPS-induced barrier hyperpermeability, monocyte adhesion, and migration. These inhibitory effects were significantly correlated with the inhibitory functions of phloroglucinol on LPS-induced cell adhesion molecules. Furthermore, LPS-induced nuclear factor-κB (NF-κB) and tumor necrosis factor-κB (TNF-κB) release from human umbilical vein endothelial cells (HUVECs) was inhibited by phloroglucinol. Given these results, phloroglucinol could be a candidate as a therapeutic agent for various systemic inflammatory diseases.
KW - Barrier integrity
KW - Cell adhesion molecule
KW - LPS
KW - Phloroglucinol
UR - http://www.scopus.com/inward/record.url?scp=84863797881&partnerID=8YFLogxK
U2 - 10.1007/s10753-011-9394-5
DO - 10.1007/s10753-011-9394-5
M3 - Article
C2 - 21976128
AN - SCOPUS:84863797881
SN - 0360-3997
VL - 35
SP - 920
EP - 926
JO - Inflammation
JF - Inflammation
IS - 3
ER -