Ginsenoside Rb1 prevents homocysteine-induced EPC dysfunction via VEGF/p38MAPK and SDF-1/CXCR4 activation.
作者： Tao-Hua Lan , Dan-Ping Xu , Man-Ting Huang , Ju-Xian Song , Huan-Lin Wu
DOI: 10.1038/S41598-017-13436-7
关键词:
摘要: 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, role Rb1 in Hcy-induced dysfunction progenitor cells (EPCs) remains unknown. In study, we found reversed impairment adhesive and migratory ability EPCs which were significantly abolished by CXCR4 antagonist AMD3100 VEGFR2 inhibitor SU5416. Ginsenoside SDF-1 reduction supernatant serum. downregulation protein expression, inhibition p38MAPK phosphorylation induced Hcy. Re-endothelialization balloon-injured carotid arteries increased with transplant, was even better treatment. This effect AMD3100. also decreased number CM-DiI labeled injured arteries. Here show first time EPC via VEGF/p38MAPK SDF-1/CXCR4 activation. These findings demonstrate a novel mechanism action may have value prevention HHcy associated
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