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Inhibitory effects of dry‐roasted licorice extract on high glucose‐induced endothelial dysfunction
Author(s) -
Choi YeanJung,
Lim Soon Sung,
Kang YoungHee
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a580-c
Subject(s) - mannitol , endothelial dysfunction , endothelial stem cell , chemistry , endothelium , viability assay , medicine , endocrinology , western blot , pharmacology , polyol pathway , diabetes mellitus , biochemistry , cell , in vitro , gene , aldose reductase
Uncontrolled hyperglycemia is the main risk factor in the development of diabetic vascular complications. The vascular lesions characteristic of human and experimental diabetes suggest a primary involvement of vascular endothelium. We tested in the present study the hypothesis that dry‐roasted licorice ethanol extract (DL) inhibit high‐glucose‐induced endothelial dysfunction in human endothelial vascular cells (HUVEC). HUVEC were cultured with 5.5 mM low‐glucose, 5.5 mM glucose plus 27.5 mM mannitol as an osmotic control, 33 mM high‐glucose for 5 days in the absence and presence of 10 μg/mL DL. Cell survival of HUVEC treated with high glucose was markedly decreased relative to that with low glucose. DL enhanced cell viability with a reduction in the high glucose‐induced nuclear condensation. High glucose caused an increase in formation of oxidants and expression of endothelial nitric oxide synthase, detected by DCF‐fluorescence and by Western blot analysis. DL substantially suppressed these detrimental effects of high glucose. We also found a role of nuclear factor‐κB (NF‐κB) in the endothelial damage under high glucose conditions. It was shown that DL interfered with NF‐κB‐dependent mechanisms under glucose‐toxic conditions. These results demonstrate that DL may be beneficial for improving the endothelial dysfunction induced by hyperglycemic and diabetic vascular complications. The detailed mechanisms involved in inhibition of endothelial injury by licorice components should be further elucidated.