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PMID:16518841
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| Citation |
Zhang, HS and Wang, SQ (2006) Ginsenoside Rg1 inhibits tumor necrosis factor-alpha (TNF-alpha)-induced human arterial smooth muscle cells (HASMCs) proliferation. J. Cell. Biochem. 98:1471-81 |
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| Abstract |
In China, the ginseng root began to be used in medicine over 2000 years ago. Ginsenosides are the most important component isolated from ginseng. The aim of this study was to determine the effects of ginsenoside Rg1 on the proliferation and molecular mechanism in cultured human arterial vascular smooth muscle cell (HASMC) induced by tumor necrosis factor-alpha (TNF-alpha). It was shown that ginsenoside Rg1 significantly inhibited TNF-alpha-induced HASMC proliferation in a dose-dependent manner. Treatment with ginsenoside Rg1, which blocked the cell cycle in the G1-phase, induced a downregulation of cyclin D1 and an upregulation in the expression of p53, p21(WAF/CIP1), and p27(KIP1). MEK inhibitors PD98059, U0126, and phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin, but not p38-inhibitor SB203580 or JNK-inhibitor SP600125 significantly aggravated ginsenoside Rg1-inhibited HASMC proliferation. Ginsenoside Rg1 markedly inactivated the extracellular signal-regulated kinases (ERK1/2) and protein kinase B (PKB), indicating that the inhibition of ginsenoside Rg1 on HASMC proliferation was associated with ERK and PI3K/PKB pathways. The inactivation of ERK and PI3K/PKB pathways and modulation of cell-cycle proteins by ginsenoside Rg1 may be of importance in inhibition of HASMCs proliferation. |
| Links |
PubMed Online version:10.1002/jcb.20799 |
| Keywords |
Cell Line; Cell Proliferation; Cyclin D1/metabolism; Cyclin-Dependent Kinase Inhibitor p21/metabolism; Cyclin-Dependent Kinase Inhibitor p27/metabolism; Dose-Response Relationship, Drug; Drug Synergism; Enzyme Inhibitors/pharmacology; G1 Phase; Ginsenosides/pharmacology; Humans; Muscle, Smooth/blood supply; Protein Kinase Inhibitors/pharmacology; RNA, Messenger/metabolism; Signal Transduction; Tumor Necrosis Factor-alpha/antagonists & inhibitors; Tumor Necrosis Factor-alpha/pharmacology; Tumor Suppressor Protein p53/metabolism |
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