PMID- 19060916
OWN - NLM
STAT- MEDLINE
DCOM- 20090421
LR  - 20231110
IS  - 1745-7254 (Electronic)
IS  - 1671-4083 (Print)
IS  - 1671-4083 (Linking)
VI  - 30
IP  - 1
DP  - 2009 Jan
TI  - Dehydroepiandrosterone anti-atherogenesis effect is not via its conversion to 
      estrogen.
PG  - 42-53
LID - 10.1038/aps.2008.2 [doi]
AB  - AIM: This study was conducted to demonstrate the anti-atherosclerotic effect of 
      dehydroepiandrosterone (DHEA) and to investigate its possible mechanisms and 
      whether this effect is related to its conversion to estrogen. METHODS: Forty male 
      New Zealand White rabbits aged 3 months were divided into 5 groups (n=8 per 
      group) and fed different diets for 10 weeks. Serum lipid levels, the area of 
      atherosclerotic lesions and the mRNA levels of monocyte chemoattractant protein-1 
      (MCP-1) and vascular cell adhesion molecule-1 (VCAM-1) in aortic lesions were 
      measured. Then cultured vascular smooth muscle cells (VSMCs) stimulated by 
      oxidized low density lipoprotein-cholesterol (ox-LDL) were treated by DHEA. The 
      gene and protein expression levels of MCP-1 and VCAM-1 in VSMCs was detected. The 
      plasmid with or without the gene of cytochrome P450 aromatase (CYP19) was 
      transient transfected into cultured VSMCs respectively. Twenty hours later, the 
      cells were stimulated with ox-LDL and DHEA. RESULTS: DHEA could obviously 
      decrease the area of atherosclerotic lesions and the expressions of MCP-1 and 
      VCAM-1 in aortic lesions. But all-trans retinoic acid (atRA) which was reported 
      would limit restenosis after balloon angioplasty had no visible synergistic 
      effect with DHEA. DHEA could also reduce ox-LDL-induced MCP-1 and VCAM-1 
      expression in untransfected or transfected VSMCs. CONCLUSION: The 
      anti-atherosclerotic effect of DHEA had nothing to do with the catalysis of 
      cytochrome P450 aromatase (CYP19), or was not related to its conversion to 
      estrogen.
FAU - Cheng, Heng-hui
AU  - Cheng HH
AD  - Institude of Pathology, Tongji Hospital, Huazhong University of Science and 
      Technology, Wuhan 430030, China.
FAU - Hu, Xiao-jing
AU  - Hu XJ
FAU - Ruan, Qiu-rong
AU  - Ruan QR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20081208
PL  - United States
TA  - Acta Pharmacol Sin
JT  - Acta pharmacologica Sinica
JID - 100956087
RN  - 0 (Chemokine CCL2)
RN  - 0 (Estrogens)
RN  - 0 (Lipids)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 0 (oxidized low density lipoprotein)
RN  - 459AG36T1B (Dehydroepiandrosterone)
SB  - IM
MH  - Animals
MH  - Arteries/anatomy & histology/metabolism
MH  - Atherosclerosis/*metabolism/pathology/physiopathology
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics/metabolism
MH  - Dehydroepiandrosterone/*metabolism/pharmacology
MH  - Diet
MH  - Estrogens/*metabolism
MH  - Humans
MH  - Lipids/blood
MH  - Lipoproteins, LDL/metabolism
MH  - Male
MH  - Muscle, Smooth, Vascular/cytology
MH  - Myocytes, Smooth Muscle/cytology/drug effects/physiology
MH  - Rabbits
MH  - Vascular Cell Adhesion Molecule-1/genetics/metabolism
PMC - PMC4006531
EDAT- 2008/12/09 09:00
MHDA- 2009/04/22 09:00
PMCR- 2009/01/01
CRDT- 2008/12/09 09:00
PHST- 2008/12/09 09:00 [pubmed]
PHST- 2009/04/22 09:00 [medline]
PHST- 2008/12/09 09:00 [entrez]
PHST- 2009/01/01 00:00 [pmc-release]
AID - aps20082 [pii]
AID - 10.1038/aps.2008.2 [doi]
PST - ppublish
SO  - Acta Pharmacol Sin. 2009 Jan;30(1):42-53. doi: 10.1038/aps.2008.2. Epub 2008 Dec 
      8.