中文摘要：

目的：研究在H2O2诱导发生的肝细胞（L-02）的氧化损伤过程中,胡黄连苷Ⅱ对抗氧化通路Keap1_Nrf2（ARE）信号蛋白的m RNA表达的影响。方法：用不同浓度胡黄连苷Ⅱ（0.5、5mmol/L）处理人正常肝细胞株（L-02）3h后,加入0.6mmol/L的H2O2作用1h造成氧化应激损伤,同时设对照组,采用荧光探针2,,7,-二氯荧光黄双乙酸盐（DCFH-DA）检测细胞内活性氧的含量,于24和48h通过实时荧光定量PCR技术检测各组细胞的Kelch样ECH相关蛋白1（Keap1）,核转录因子E2相关因子（Nrf2）和血红素加氧酶-1（HO-1）蛋白的m RNA的表达情况。结果：胡黄连苷Ⅱ预处理后,肝细胞内活性氧含量较模型组（仅H2O2作用后）明显减少（P〈0.05）,药物高浓度干预组Nrf2、HO-1的m RNA表达较模型组显著增高（P〈0.05）,且随浓度的提高而增加。结论：通过影响抗氧化通路Keap1_Nrf2（ARE）,增加下游抗氧化蛋白表达,清除细胞内活性氧,可能是胡黄连苷Ⅱ发挥保护H2O2诱导的肝细胞损伤作用机制之一。

英文摘要：

Objective： To study the effects of picroside Ⅱ on the mRNA expression of Keapl_Nrf2 （ARE） antioxidant signal pathway in liver cells induced by H2O2 in vitro. Methods： L-02 cells were treated with picroside Ⅱ at different concentration （0, 0.5, 5mmol/L） for three hour, and then injured by H202 （0.6mmol/L） for one hour. The control group was set at the same time. The content of reactive oxygen species （ROS） was detected by the fluorescent probe 2＇,7＇-dichlorodihydrofluorescein diacetate （DCFH-DA）. The mRNA expression of Keapl, Nrf2 and HO-1 genes was detected by using RT-PCR at the 24th and 48th hour. Results： Compared with the model group （only after treatment with H202）, the content of ROS in the L-02 cells treated with the picroside ]l was decreased obviously （P〈0.05）, while the mRNA expression of Nrf2, HO-1 was increased （P〈0.05）, and increased with increasing concentration. Conclusion： The expression of downstream antioxidant protein is increased, cleared intracellular reactive oxygen species through affect the antioxidant pathway Keapl_Nrf2 （ARE）, and it might make picroside Ⅱ play a protective role in the mechanism of liver cells damage induced by H2O2.