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An ethanol extract of Buddleia officinalis suppresses high glucose‐induced vascular smooth muscle cell proliferation
Author(s) -
Lee Yun Jung,
Kang Dae Gill,
Moon Mi Kyoung,
Cao Li Hua,
Hwang Sun Mi,
Kim Jin Sook,
Lee Ho Sub
Publication year - 2008
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.22.1_supplement.912.41
Subject(s) - vascular smooth muscle , cell growth , p38 mitogen activated protein kinases , chemistry , medicine , endocrinology , matrix metalloproteinase , phosphorylation , smooth muscle , biochemistry , biology , mapk/erk pathway
Diabetes mellitus is a well‐established risk factor for vascular diseases caused by atherosclerosis. In the development of diabetic atherogenesis, vascular smooth muscle cell proliferation is recognized as a key event. Thus, we aimed to investigate whether an ethanol extract of Buddleia officinalis (EBO) suppresses high glucose‐induced proliferation in primary cultured human aortic smooth muscle cells (HASMC). [ 3 H]‐thymidine incorporation and MTT assay revealed that incubation of HASMC with high concentration of glucose (25 mM) increased cell proliferation. The expression levels of cell cycle protein were also increased by treatment with high glucose. Pretreatment of HASMC with EBO significantly attenuated the increase of high glucose‐induced cell proliferation. EBO also suppressed p38 and JNK phosphorylation. EBO suppressed high glucose‐induced matrix metalloproteinase (MMP)‐2/9 expressions and activities in dose‐dependent manner. In addition, EBO suppressed NF‐κB promoter transcriptional activity in a high glucose condition. Taken together, the present data suggested that EBO could suppress high glucose‐induced atherosclerotic processes via inhibition of p38, JNK, NF‐κB, and MMPs signal pathways in HASMC.