PMID- 22687414
OWN - NLM
STAT- MEDLINE
DCOM- 20121015
LR  - 20190720
IS  - 1347-5215 (Electronic)
IS  - 0918-6158 (Linking)
VI  - 35
IP  - 5
DP  - 2012
TI  - Paeonol inhibits oxidized low density lipoprotein-induced monocyte adhesion to 
      vascular endothelial cells by inhibiting the mitogen activated protein kinase 
      pathway.
PG  - 767-72
AB  - Atherosclerosis is a chronic inflammatory disease characterized by increased 
      expression of adhesion molecules, which contribute to monocytes adhesion to 
      vascular endothelial cells (VECs). Paeonol, an active compound isolated from 
      cortex Moutan, has been shown to have therapeutic effects on atherosclerotic 
      animals. The present study aims to investigate whether paeonol can inhibit 
      monocyte adhesion to vascular endothelial cells induced by oxidized Low-Density 
      Lipoprotein (ox-LDL) and its possible therapeutic molecular mechanism. Exposure 
      to ox-LDL (50, 100 microg/mL) induced damaged to VECs leading to decreased survival 
      rates (p<0.01). Paeonol (7.2-18.0 microM) partially restored survival and reduced 
      lactate dehydrogenase (LDH) release in VECs in a concentration-dependent manner 
      (p<0.01). Adhesion of monocytes to VECs was dramatically prevented by paeonol at 
      21.6 and 25.2 muM (p<0.01). In addition, paeonol (14.4-21.6 muM) repressed the 
      expression of vascular cell adhesion molecule-1 (VCAM-1) and lowered the levels 
      of phosphor-c-Jun N-terminal kinase (P-JNK)1/2, phosphor-extracellular 
      signal-regulated kinase (P-ERK)1/2 and P-p38 in a dose-dependent manner. The 
      molecular effects of paeonol were more pronouced when companied with mitogen 
      activated protein kinases (MAPKs) inhibitors. These data suggest that paeonol 
      (10.8-25.2 muM), at certain concentrations, prevents monocyte adhesion to VEC 
      induced by ox-LDL, probably by means of blocking one or more target proteins on 
      MAPKs signaling pathway. These results indicate that paeonol has potential 
      protective effects on the development of atherosclerosis.
FAU - Wang, Yue-Qin
AU  - Wang YQ
AD  - Key Laboratory of Xin'an Medicine, Ministry of Education, Experimental Center for 
      Scientific Research, Hefei, Anhui, China.
FAU - Dai, Min
AU  - Dai M
FAU - Zhong, Ji-Chang
AU  - Zhong JC
FAU - Yin, Deng-Ke
AU  - Yin DK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Japan
TA  - Biol Pharm Bull
JT  - Biological & pharmaceutical bulletin
JID - 9311984
RN  - 0 (Acetophenones)
RN  - 0 (Drugs, Chinese Herbal)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 0 (oxidized low density lipoprotein)
RN  - 3R834EPI82 (paeonol)
RN  - EC 1.1.1.27 (L-Lactate Dehydrogenase)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Acetophenones/*pharmacology/therapeutic use
MH  - Animals
MH  - Atherosclerosis/drug therapy/*metabolism
MH  - Cell Adhesion/drug effects
MH  - Dose-Response Relationship, Drug
MH  - Drugs, Chinese Herbal/pharmacology/therapeutic use
MH  - Endothelial Cells/*drug effects/metabolism
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - JNK Mitogen-Activated Protein Kinases/metabolism
MH  - L-Lactate Dehydrogenase/metabolism
MH  - Lipoproteins, LDL/*metabolism
MH  - Mitogen-Activated Protein Kinases/*antagonists & inhibitors
MH  - Monocytes/cytology/*drug effects
MH  - Paeonia/*chemistry
MH  - Phytotherapy
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction/drug effects
MH  - Vascular Cell Adhesion Molecule-1/metabolism
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
EDAT- 2012/06/13 06:00
MHDA- 2012/10/16 06:00
CRDT- 2012/06/13 06:00
PHST- 2012/06/13 06:00 [entrez]
PHST- 2012/06/13 06:00 [pubmed]
PHST- 2012/10/16 06:00 [medline]
AID - JST.JSTAGE/bpb/35.767 [pii]
AID - 10.1248/bpb.35.767 [doi]
PST - ppublish
SO  - Biol Pharm Bull. 2012;35(5):767-72. doi: 10.1248/bpb.35.767.