Open AccessEffects of Resveratrol on Endothelial Progenitor Cells and Their Contributions to Reendothelialization in Intima-injured Rats
Author(s) -
Jieruo Gu,
Wang Cq,
Fan Hh,
Haiyan Ding,
Xie Xl,
Xu Ym,
Wang By,
Huang Dj
Publication year - 2006
Publication title -
journal of cardiovascular pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.762
H-Index - 100
eISSN - 1533-4023
pISSN - 0160-2446
DOI - 10.1097/01.fjc.0000211764.52012.e3
Subject(s) - enos , resveratrol , progenitor cell , endothelial progenitor cell , aorta , restenosis , in vitro , chemistry , endothelial stem cell , pharmacology , endothelium , medicine , nitric oxide , stem cell , biology , microbiology and biotechnology , nitric oxide synthase , biochemistry , stent
The aim of this study was to investigate the effects of resveratrol on endothelial progenitor cell (EPC) activities in vitro and on the mobilization of circulating EPCs, and reendothelialization in balloon-injured aorta of rats. After being isolated, cultured, and characterized, human EPCs were stimulated with resveratrol. We found that a low concentration of resveratrol (1 microM) led to significant enhanced activities of proliferation, migration, and adhesion, as well as promoting endothelial nitric acid synthetase (eNOS) expression in EPCs, whereas a high concentration (60 microM) inhibited the aforementioned functions and eNOS expression. In a rat model of injured aorta, a low dosage of resveratrol (10 mg/kg) increased the amount of EPCs in rat circulation as compared with placebo, whereas the result of a high dosage (50 mg/kg) did not reach statistical difference. In addition, 10 mg/kg of resveratrol both accelerated reendothelialization and inhibited neointimal formation; however, 50 mg/kg only reduced neointimal formation, which was not as effective as the previous one. eNOS expression in injured arteries was potently enhanced in the 10 mg/kg group, but not in the 50 mg/kg group. These findings suggest that a low dosage of resveratrol could markedly raise the proliferative, migrative, and adhesive activities of EPCs and upgrade eNOS expression in vitro as well as increase EPC mobilization, enhance eNOS expression, and accelerate the repair of injured artery; however, a high dosage cannot.