PMID- 24792192
OWN - NLM
STAT- MEDLINE
DCOM- 20150126
LR  - 20220330
IS  - 1879-3649 (Electronic)
IS  - 1537-1891 (Linking)
VI  - 62
IP  - 1
DP  - 2014 Jul
TI  - Vascular barrier protective effects of orientin and isoorientin in LPS-induced 
      inflammation in vitro and in vivo.
PG  - 3-14
LID - S1537-1891(14)00078-0 [pii]
LID - 10.1016/j.vph.2014.04.006 [doi]
AB  - Endothelial cell protein C receptor (EPCR) can be shed from the cell surface, and 
      this process is mediated by tumor necrosis factor-alpha converting enzyme (TACE), and 
      high levels of soluble EPCR are involved in vascular inflammation. Orientin, one 
      of the C-glycosyl flavonoids, has been known to have anxiolytic and antioxidative 
      activities. However, the effect of orientin on lipopolysaccharide (LPS)-induced 
      inflammatory response has not been studied. Here we investigated the barrier 
      protective effects of orientin against pro-inflammatory responses induced by LPS 
      and the associated signaling pathways. We found that orientin inhibited 
      LPS-induced barrier disruption, expression of cell adhesion molecules (CAMs), and 
      adhesion/transendothelial migration of monocytes to human endothelial cells. 
      Orientin induced potent inhibition of phorbol-12-myristate 13-acetate (PMA) and 
      LPS-induced EPCR shedding. Orientin also suppressed LPS-induced hyperpermeability 
      and leukocyte migration in vivo. Furthermore, orientin suppressed the production 
      of tumor necrosis factor-alpha (TNF-alpha) or Interleukin (IL)-6 and the activation of 
      nuclear factor-kappaB (NF-kappaB) or extracellular regulated kinases (ERK) 1/2 by LPS. 
      Moreover, treatment with orientin resulted in reduced LPS-induced lethal 
      endotoxemia. These results suggest that orientin protects vascular barrier 
      integrity by inhibiting hyperpermeability, expression of CAMs, and adhesion and 
      migration of leukocytes, thereby endorsing its usefulness as a therapy for 
      vascular inflammatory diseases.
CI  - Copyright (c) 2014 Elsevier Inc. All rights reserved.
FAU - Lee, Wonhwa
AU  - Lee W
AD  - College of Pharmacy, CMRI, Research Institute of Pharmaceutical Sciences, 
      Kyungpook National University, Daegu 702-701 Republic of Korea; BK21 Plus KNU 
      Biomedical Convergence Program, Department of Biochemistry and Cell Biology, 
      School of Medicine, Kyungpook National University, Daegu 702-701 Republic of 
      Korea.
FAU - Ku, Sae-Kwang
AU  - Ku SK
AD  - Department of Anatomy and Histology, College of Korean Medicine, Daegu Haany 
      University, Gyeongsan 712-715, Republic of Korea.
FAU - Bae, Jong-Sup
AU  - Bae JS
AD  - College of Pharmacy, CMRI, Research Institute of Pharmaceutical Sciences, 
      Kyungpook National University, Daegu 702-701 Republic of Korea. Electronic 
      address: baejs@knu.ac.kr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140502
PL  - United States
TA  - Vascul Pharmacol
JT  - Vascular pharmacology
JID - 101130615
RN  - 0 (Antigens, CD)
RN  - 0 (Antioxidants)
RN  - 0 (E-Selectin)
RN  - 0 (Endothelial Protein C Receptor)
RN  - 0 (Endotoxins)
RN  - 0 (Flavonoids)
RN  - 0 (Glucosides)
RN  - 0 (PROCR protein, human)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 67924-63-4 (endotoxin, Escherichia coli)
RN  - A37342TIX1 (homoorientin)
RN  - IAX93XCW6C (orientin)
RN  - KUX1ZNC9J2 (Luteolin)
SB  - IM
MH  - Animals
MH  - Antigens, CD/metabolism
MH  - Antioxidants/administration & dosage/*therapeutic use
MH  - Capillary Permeability/*drug effects
MH  - Cell Adhesion/drug effects
MH  - Cell Movement/drug effects
MH  - Cell Survival/drug effects
MH  - Dose-Response Relationship, Drug
MH  - E-Selectin/biosynthesis
MH  - Endothelial Protein C Receptor
MH  - Endothelium, Vascular/*drug effects/immunology/metabolism
MH  - Endotoxins/pharmacology
MH  - Flavonoids/administration & dosage/*therapeutic use
MH  - Glucosides/administration & dosage/*therapeutic use
MH  - Human Umbilical Vein Endothelial Cells
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/biosynthesis
MH  - Luteolin/administration & dosage/*therapeutic use
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Monocytes/cytology
MH  - Receptors, Cell Surface/metabolism
MH  - Vascular Cell Adhesion Molecule-1/biosynthesis
MH  - Vasculitis/chemically induced/*drug therapy/immunology/physiopathology
OTO - NOTNLM
OT  - Barrier integrity
OT  - C-glycosylflavone isomer pairs
OT  - Endothelium
OT  - Inflammation
OT  - Lipopolysaccharide
EDAT- 2014/05/06 06:00
MHDA- 2015/01/27 06:00
CRDT- 2014/05/06 06:00
PHST- 2014/02/17 00:00 [received]
PHST- 2014/04/12 00:00 [revised]
PHST- 2014/04/18 00:00 [accepted]
PHST- 2014/05/06 06:00 [entrez]
PHST- 2014/05/06 06:00 [pubmed]
PHST- 2015/01/27 06:00 [medline]
AID - S1537-1891(14)00078-0 [pii]
AID - 10.1016/j.vph.2014.04.006 [doi]
PST - ppublish
SO  - Vascul Pharmacol. 2014 Jul;62(1):3-14. doi: 10.1016/j.vph.2014.04.006. Epub 2014 
      May 2.