中文摘要：

目的明确NOX对血管紧张素Ⅱ（AngⅡ）诱导的HSC转录因子激活蛋白-1（AP-1）和核因子-κB（NF-κB）的调控作用及熊果酸（UA）干预后的影响。方法将培养激活的HSC—T6细胞株分为：AngII组，给予AngⅡ（1μmol／L）刺激细胞；空白对照组：不加任何药物；各干预组分别给予UA（50μmol／L）、NOX抑制剂DPI（20μmol／L）预处理30min，再加入AngⅡ处理不同时间。采用活性氧检测试剂盒和荧光酶标仪检测其余各组细胞内荧光强度；用电泳迁移率（EMSA）测定细胞内AP-1、NF-κB的活性。结果HSC—T6经药物作用30min后，AngⅡ组DCF荧光强度比空白对照组明显升高（P〈0．05），分别给予UA、DPI干预后细胞内DCF荧光强度均显著低于AngⅡ组（P〈0．05），AngⅡ＋UA组与AngⅡ＋DPI组相比较DCF荧光强度无明显差异（P〉0．05）；用AngⅡ刺激HsC—T6细胞1h后，AngⅡ组AP-1、NF-κB的活性明显高于空白对照组（P〈0．05），分别给予UA、DPI干预后，细胞内AP-1、NF？KB的活性均显著低于AngⅡ组；AngⅡ＋UA组与AngⅡ＋DPI组相比较AP-1、NF-κB的活性无明显差异（P〉0．05）。结论NOX产生的ROS介导AngⅡ刺激HSC转录因子AP-1和NF-κB的活化，熊果酸通过抑制HSC内ROS的生成阻断AP-1、NF-κB的活化。

英文摘要：

Objective To clarify the effects of NOX on the generation of ROS and the activity of AP - 1 and NF - κB in rat hepatic stellate cells （ HSC - TS） induced by Ang Ⅱ. Methods Culture - activated HSC - T6 cells were divided as followed ： Ang Ⅱ group （ received Ang Ⅱ） ; normal control group （ received no treatment ） ; and intervention groups, in which HSC -T6 cells were pretreated with UA （50 p.moL/L） and NOX inhibitor DPI （20 μmol/L） for 30 min, and subsequently stimulated with Ang Ⅱ for different time periods. The fluorescence intensity was examined with ROS detection kit and fluorescence microplate. The activities of AP - 1 and NF - κB were determined using electrophoretic mobility shift assay （EMSA）. Results After treated with Ang Ⅱ for 30 rain, the fluorescence intensity was higher than control group （ P 〈 0. 05 ）. After intervened by DPI and UA, the fluorescence intensity was significantly lower than that in Ang Ⅱ treated groups （ P 〈 0.05 ）. After treated with Ang Ⅱ for one hour, the activities of AP - 1 and NF - κB were significantly higher than control group （ P 〈 0.05 ）. After intervened by DPI and UA, The activities of AP - 1 and NF - κB were significantly lower than that in Ang Ⅱ treated groups （ P 〈 0. 05 ）. Conclusion NOX can mediate the activation of AP - 1 and NF - κB by influencing the generation of ROS, UA Can reduce the activity of AP - 1 and NF - κB by inhibiting generation of ROS.