中文摘要：

为了探讨雌激素对H2O2诱导PC12细胞氧化损伤的影响及其可能机制.用H2O2处理PC12细胞建立氧化应激模型,并加入雌激素预处理作为保护.MTT法检测细胞活力,利用荧光探针对细胞内ROS进行荧光染色检测荧光强度,Hoechst/PI荧光染色,分析细胞凋亡情况,Western blotting检测MAPK（Mitogen-Activated Protein Kinase）的磷酸化水平.结果显示：H2O2作用于PC12细胞后显著降低细胞活力,10-8～10-6mol/L的雌激素预处理后均能部分阻断H2O2对细胞活力的影响.H2O2能显著增强PC12细胞的ROS荧光强度,雌激素可明显减少H2O2处理后PC12细胞内的ROS含量.H2O2激活MAPK,而雌激素抑制了p38的磷酸化,增加了ERK的磷酸化.以上结果表明,雌激素可以拮抗H2O2诱导的氧化应激,抑制p38的磷酸化,增强ERK的磷酸化可能是其发挥保护作用的机制之一.

英文摘要：

To investigate the neuroprotective effect of estrogen on the H2O2-induced oxidative stress in PC12 cells,oxidative damaged PC12 cells was treated by H2O2 to construct the model on the oxidative stress reaction,and estrogen was added as a pretreatment to protect the cells.The survival rate of the cells was determined by MTT method,intracellular ROS generation was detected by DCFH-DA fluorescent probe,apoptosis was analyzed by Hoechst/PI fluorescence staining,and the level of mitogen-activated protein（MAP） kinase phosphorylation was detected by the Western blotting.The results showed that：The pretreated pheochromocytoma cell line PC12 by estrogen（0.001—1 μmol/L） recovered significantly from the hydrogen peroxide（H2O2）-induced cell injury.The intensity of DCFH-DA fluorescence was significantly increased after the treatment by H2O2,indicating that ROS generation was successfully induced in PC12 cell,and estrogen（1μmol/L） decreased the DCFH-DA fluorescence intensity significantly.Estrogen suppressed H2O2-induced phosphorylation of p38MAPK and increased H2O2-induced phosphorylation of ERK1 /2.It was suggest that estrogen protected against H2O2-induced oxidative stress in vitro and its protective effect was associated with the inhibition of p38 MAPK and the activation of ERK.