中文摘要：

我们的以前的研究证明 resveratrol 能禁止脉管的光滑的肌肉房间(VSMC ) 的增长并且镇压 quinone reductase 的 mRNA 和蛋白质表示 2 (NQO2 ) 。这研究进一步探索了 resveratrol 禁止老鼠 VSMC 的增长的潜在的机制。合并了 NQO2 的 Lentiviral 向量小介入 RNA (siRNA ) 被构造并且 transduced 进老鼠 VSMC。房间增长用 bromodeoxyuridine (BrdU ) 被检测试金。有教养的老鼠 VSMC 与血管收缩素 II 被刺激，反应的氧种类(ROS ) 的水平用一个 ROS 试金工具包被测量。即时量的 PCR 被用来检测 NQO2 mRNA 层次。细胞外的调整信号的 kinase (ERK1/2 ) 和 NQO2 蛋白质表示被西方的弄污的分析决定。在 NQO2 siRNA 组的老鼠 VSMC 的增长上的 resveratrol (10 和 50 mol/L ) 的禁止的效果在正常、爬的 siRNA 组是比那显著地弱的(P < 0.01 ) 。在处理组织的 NQO2 siRNA 和 resveratrol (50 mol/L ) 的 ROS 水平在正常、爬的 siRNA 组是比那低的(P < 0.01 在两个) 。与正常、爬的 siRNA 组相比， ERK1/2 的 phosphorylation 显著地在 NQO2 siRNA 和 resveratrol (50 mol/L ) 被减少处理组(P < 0.01 在两个) 。在结论， resveratrol 的高集中禁止血管收缩素由在有教养的老鼠 VSMC 的 NQO2 的下面规定的导致 II 的 ERK1/2 phosphorylation 和随后的增长。

英文摘要：

Our previous studies showed that resveratrol could inhibit the proliferation of vascular smooth muscle cells （VSMCs） and repress mRNA and protein expression of quinone reductase 2 （NQO2）. This study further explored the potential mechanisms whereby resveratrol inhibits the proliferation of rat VSMCs. Lentiviral vectors that incorporated NQO2 small interfering RNA （siRNA） were constructed and transduced into rat VSMCs. The cell proliferation was detected using the bromodeoxyuridine （BrdU） assay. Cultured rat VSMCs were stimulated with angiotensin II and the level of reactive oxygen species （ROS） was measured using a ROS assay kit. A realtime quantitative PCR was used to detect NQO2 mRNA levels. Extracellular signal-regulated kinase （ERK1/2） and NQO2 protein expression were determined by Western blotting analysis. The inhibitory effect of resveratrol （10 and 50 μmol/L） on the proliferation of rat VSMCs in the NQO2 siRNA group was significantly weaker than that in the normal and scrambled siRNA group （P 〈 0.01）. The ROS level in the NQO2 siRNA and resveratrol （50 μmol/L） treatment groups were lower than that in the normal and scrambled siRNA groups （P 〈 0.01 in both）. Compared with the normal and scrambled siRNA group, the phosphorylation of ERK1/2 was significantly decreased in the NQO2 siRNA and resveratrol （50 μmol/L） treatment group （P 〈 0.01 in both）. In conclusion, high concentration of resveratrol inhibits angiotensin II-induced ERK1/2 phosphorylation and subsequent proliferation by down-regulation of NQO2 in cultured rat VSMCs.