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| Rutaecarpine Inhibits Angiotensin Ⅱ-Induced Proliferation in Rat Vascular Smooth Muscle Cells |
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| KeyWord:rutaecarpine, angiotensin Ⅱ, nitric oxide, vascular smooth muscle cell proliferation, gene expression |
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| Abstract: |
| Objective: To evaluate the effects and possible mechanisms of rutaecarpine on angiotensin Ⅱ (Ang Ⅱ)-induced proliferation in cultured rat vascular smooth muscle cells (VSMCs). Methods: VSMCs were isolated from Male Sprague-Dawley rat aorta, and cultured by enzymic dispersion method. Experiments were performed with cells from passages 3–8. The cultured VSMCs were randomly divided into control, model (Ang Ⅱ 0.1 μmol/L), and rutaecarpine (0.3–3.0 μmol/L) groups. VMSC proliferation was induced by Ang Ⅱ, and was evaluated by the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay and cell counting. To examine the mechanisms involved in anti-proliferative effects of rutaecarpine, nitric oxide (NO) levels and NO synthetase (NOS) activity were determined. Expressions of VSMC proliferation-related genes including endothelial nitric oxide synthase (eNOS), and c-myc hypertension related gene-1 (HRG-1) were determined by real-time reverse transcription-polymerase chain reaction (RT-PCR). Results: Rutaecarpine (0.3–3.0 μmol/L) inhibited Ang Ⅱ-induced VSMC proliferation and the best effects were achieved at 3.0 μmol/L. The Ang Ⅱ-induced decreases in cellular NO contents and NOS activities were antagonized by rutaecarpine (P<0.05). Ang Ⅱ administration suppressed the expressions of eNOS and HRG-1, while increased c-myc expression (P<0.05). All these effects were attenuated by 3.0 μmol/L rutaecarpine (P<0.05). Conclusion: Rutaecarpine is effective against Ang Ⅱ-induced rat VSMC proliferation, and this effect is due, at least in part, to NO production and the modulation of VMSC proliferation-related gene expressions. |
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