PMID- 29026158
OWN - NLM
STAT- MEDLINE
DCOM- 20190701
LR  - 20211204
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 7
IP  - 1
DP  - 2017 Oct 12
TI  - Ginsenoside Rb1 prevents homocysteine-induced EPC dysfunction via VEGF/p38MAPK 
      and SDF-1/CXCR4 activation.
PG  - 13061
LID - 10.1038/s41598-017-13436-7 [doi]
LID - 13061
AB  - Hyperhomocystinemia (HHcy) is known as an independent risk factor for 
      cardiovascular disease. Our previous study showed that ginsenoside Rb1, the major 
      active constituent of ginseng, prevents homocysteine (Hcy)-induced endothelial 
      damage. However, the role of ginsenoside Rb1 in Hcy-induced dysfunction in 
      endothelial progenitor cells (EPCs) remains unknown. In the study, we found that 
      ginsenoside Rb1 reversed the Hcy-induced impairment of adhesive and migratory 
      ability in EPCs which were significantly abolished by CXCR4 antagonist AMD3100 
      and VEGFR2 inhibitor SU5416. Ginsenoside Rb1 significantly reversed Hcy-induced 
      SDF-1 reduction in the supernatant and in the serum. Ginsenoside Rb1 reversed 
      downregulation of SDF-1 and VEGFR2 protein expression, inhibition of p38MAPK 
      phosphorylation induced by Hcy. Re-endothelialization in balloon-injured carotid 
      arteries significantly increased with EPCs transplant, and was even better with 
      Rb1 treatment. This effect was significantly abolished by AMD3100. AMD3100 also 
      decreased the number of CM-DiI labeled EPCs in injured arteries. Here we show for 
      the first time that Rb1 prevents Hcy-induced EPC dysfunction via VEGF/p38MAPK and 
      SDF-1/CXCR4 activation. These findings demonstrate a novel mechanism of the 
      action of Rb1 that may have value in prevention of HHcy associated cardiovascular 
      disease.
FAU - Lan, Tao-Hua
AU  - Lan TH
AD  - Department of Cardiology, The Second Affiliated Hospital of Guangzhou University 
      of Chinese Medicine, Guangzhou, P. R. China.
AD  - School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, Hong Kong.
FAU - Xu, Dan-Ping
AU  - Xu DP
AD  - Department of Cardiology, The Second Affiliated Hospital of Guangzhou University 
      of Chinese Medicine, Guangzhou, P. R. China.
FAU - Huang, Man-Ting
AU  - Huang MT
AD  - Department of Cardiology, The Second Affiliated Hospital of Guangzhou University 
      of Chinese Medicine, Guangzhou, P. R. China.
FAU - Song, Ju-Xian
AU  - Song JX
AD  - School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, Hong Kong.
FAU - Wu, Huan-Lin
AU  - Wu HL
AD  - Department of Cardiology, The Second Affiliated Hospital of Guangzhou University 
      of Chinese Medicine, Guangzhou, P. R. China. heart-center2@gzucm.edu.cn.
FAU - Li, Min
AU  - Li M
AD  - School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, Hong Kong. 
      limin@hkbu.edu.hk.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171012
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
RN  - 0 (Benzylamines)
RN  - 0 (Chemokine CXCL12)
RN  - 0 (Cyclams)
RN  - 0 (Ginsenosides)
RN  - 0 (Heterocyclic Compounds)
RN  - 0 (Indoles)
RN  - 0 (Pyrroles)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 71IA9S35AJ (Semaxinib)
RN  - 7413S0WMH6 (ginsenoside Rb1)
RN  - EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-2)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - S915P5499N (plerixafor)
SB  - IM
MH  - Animals
MH  - Benzylamines
MH  - Cell Movement/drug effects
MH  - Cell Survival/drug effects
MH  - Chemokine CXCL12/blood/metabolism
MH  - Cyclams
MH  - Endothelial Progenitor Cells/*drug effects/*metabolism
MH  - Ginsenosides/*pharmacology
MH  - Heterocyclic Compounds/pharmacology
MH  - Homocysteine/*pharmacology
MH  - Indoles/pharmacology
MH  - Male
MH  - Phosphorylation/drug effects
MH  - Pyrroles/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Vascular Endothelial Growth Factor A/blood/*metabolism
MH  - Vascular Endothelial Growth Factor Receptor-2/blood/metabolism
MH  - p38 Mitogen-Activated Protein Kinases/blood/*metabolism
PMC - PMC5638839
COIS- The authors declare that they have no competing interests.
EDAT- 2017/10/14 06:00
MHDA- 2019/07/02 06:00
PMCR- 2017/10/12
CRDT- 2017/10/14 06:00
PHST- 2017/03/29 00:00 [received]
PHST- 2017/09/25 00:00 [accepted]
PHST- 2017/10/14 06:00 [entrez]
PHST- 2017/10/14 06:00 [pubmed]
PHST- 2019/07/02 06:00 [medline]
PHST- 2017/10/12 00:00 [pmc-release]
AID - 10.1038/s41598-017-13436-7 [pii]
AID - 13436 [pii]
AID - 10.1038/s41598-017-13436-7 [doi]
PST - epublish
SO  - Sci Rep. 2017 Oct 12;7(1):13061. doi: 10.1038/s41598-017-13436-7.