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Ugonin J, a bioactive compound isolated from Helminthostachys zeylanica (L) Hook. (Helminthostachyaceae), demonstrates inhibitory effects on neointima formation in the rat carotid artery
Author(s) -
Wu ChiehHsi,
Yeh WanTing,
Li PeiChung
Publication year - 2013
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.27.1_supplement.922.11
Subject(s) - neointima , restenosis , neointimal hyperplasia , vascular smooth muscle , matrix metalloproteinase , medicine , pi3k/akt/mtor pathway , protein kinase b , stent , microbiology and biotechnology , smooth muscle , biology , signal transduction
The clinical value of percutaneous coronary angioplasty (PTCA) for treating arterial obstruction has always been counteracted by neointimal hyperplasia. Development of restenosis has been attributed to abnormal proliferation and migration of vascular smooth muscle cells (VSMCs). The purpose of the present study was to investigate whether Ugonin J, a bioactive compound isolated from Helminthostachys zeylanica (L) Hook. (Helminthostachyaceae), has potential effects to prevent neointimal formation, and to explore its molecular mechanisms. Our current findings demonstrated that at 12, 24 and 36 μM Ugonin J markedly inhibited cell growth and migration of VSMCs (A7r5). Cytometric analysis suggested that Ugonin J arrest VSMCs in the G1 phase at 36 μM. Ugonin J was able to suppress the activities of matrix metalloproteinase (MMP)‐2 and MMP‐9 in a concentration‐dependent manner. Ugonin J was also found to decrease the expression levels of p‐AKT, p‐ERK1/2, p‐FAK, ERP57, PGK1, PI3K and MMP‐2 and MMP‐9, whereas the total protein levels of AKT, ERK1/2 and FAK were not significantly changed. Our data demonstrated that Ugonin J can be a potential regulator to inhibit cell migration and neointimal formation in clinical restenosis after PTCA.