中文摘要：

目的：研究熊果酸对经氧化性低密度脂蛋白（ox—LDL）干预后人脐静脉血管内皮细胞（human umbilical vein endothelial cells，HUVECs）醌还原氧化酶1表达的影响，以进一步探讨熊果酸抗动脉粥样硬化的机制。方法：体外培养人脐静脉内皮细胞，进行分组处理，每组n=5。对照组，不加任何处理；ox—LDL组，加入ox—LDL培养24h，终浓度为20mg／L；ox—LDL＋低浓度熊果酸组，先加入ox-LDL（浓度20mg／L）孕育半小时，然后与熊果酸（浓度1．5μmlo／L）共同培养24h；ox-LDL＋高浓度熊果酸组，先加入ox—LDL（浓度20mg／L）孕育半小时，然后与熊果酸（浓度4．5μmlo／L）共同培养24h；采用MTT试验测定细胞吸光度值，检测熊果酸对OX—LDL损伤的保护作用，采用RT-PCR法检测NQO1mRNA的表达，采用Westemblot法检测NQ01蛋白的表达。结果：熊果酸减弱ox-LDL对HUVECs的损伤作用；ox—LDL组NQO1mRNA的表达量（0．624±0．009）明显高于对照组（0．521±0．007），P〈0．01。熊果酸呈浓度依赖性的提高NQ01mRNA的表达量（ox-LDL＋低浓度熊果酸组vs ox-LDL组：0．722±0．058VS0．624±0．009，P〈0．01；ox—LDL＋高浓度熊果酸组vs ox—LDL组：0．826±0．059VS0．624±0．009，P〈0．01）。ox-LDL组NQ01蛋白的表达量（0．624±0．009）明显高于对照组（0．521±0．007），P〈0．01。熊果酸呈浓度依赖性的提高NQ01蛋白的表达量（ox-LDL＋低浓度熊果酸组vs ox-LDL组：0．710±0．058 vs 0．574±0．024，P〈0．01；ox—LDL＋高浓度熊果酸组vs ox—LDL组：0．831±0．034 vs 0．574±0．024，P〈0．01）。结论：熊果酸可上调ox-LDL诱导的人脐静脉血管内皮细胞NQ01的表达，表明其可能具有抗氧化应激及抗动脉粥样硬化的作用。

英文摘要：

Objective： To investigate the effects of Ursolic acid on NQO1 （Quinone Oxidoreductasel, NQO1）incultured umbilical vein endothelial cells （HUVECs） stimulated by ox-LDL, so as to approach the mechanism of UA in atherosclerosis. Methods： HUVECs were cultured in different concentration and divided into four groups （n=5,each）： Group Ⅰ, control group without; Group Ⅱ, HUVECs stimulated with ox-LDL （20 mg/L） in endothelial basal medium for 24 hours; GrouplⅢ, HUVECs treated with ox-LDL（20m g/L） for an half hours, and treated with ox-LDL （20 mg/L） and UA （1.5 μmol/L） in endothelial basal medium for 24 hours; GrouplV, HUVECs treated with ox-LDL（20 mg/L） for an half hours, and treated with ox-LDL （20 mg/L） and UA （4.5μmol/L） in endothelial basal medium for 24 hours. MTT assay was used to determine against HUVECs injury. Expression of NQOlmRNA was determined by RT-PCR. Expression of NQO1 protein was determined by Western blot. Results： Ursolic acid decreased the effect on reducing the cytotoxicity of ox- LDL. Expression of NQOlmRNA was significantly highter in group Ⅱ （0.624± 0.009）than that in group Ⅰ （0.521± 0.007）, P〈0.01. Ursolic acid dose-dependenly increased expression of NQO1 mRNA （GroupⅢvs Group Ⅱ ： 0.722：1：0.058 vs 0.624± 0.009, P〈0.01; Group IV vs Group Ⅱ ： 0.826 ± 0.059 vs 0.624 ± 0.009, P〈0.01）. Expression of NQO1 Protein was significantly highter in group Ⅱ （0.574± 0.024）than that in group Ⅰ （0.438± 0.039）, P〈0.01. Ursolic acid dose-dependenly increased expression of NQO1 Protein（Group Ⅲvs Group Ⅱ ： 0.710± 0.058 vs 0.574± 0.024, P〈0.01; Group Ⅳ vs Group Ⅱ ： 0.831± 0.034 vs 0.574± 0.024, P〈0.01）. Conclusion： NQO1 expression in ox-LDL-treated HUVECs could be increased by UA which suggests that UA may attenuate atherosclerosis by re-ducing ox-LDL-induced oxidative stress responses.