大黄素甲醚对PC12细胞缺氧损伤的保护作用

目的探讨大黄素甲醚对PC12细胞缺氧损伤的影响。方法体外培养PC12细胞，缺氧处理后给予小同溶浓度大黄素甲醚下预；四甲基偶氮唑盐（MTT）法检测PCI2细胞增殖活性的变化，油镜观察PC12细胞核形态变化，测定上清液中超氧化物歧化酶（SOD）含量，PCR分析丝裂原活化蛋白激酶p38（p38MAPK）和半胱氨酸蛋白酶-3（Caspase-3）的表达。结果缺氧24h后，大黄素甲醚干预后细胞核形态较清楚，偶有肿胀皱缩，少见颗粒样物质形成；大黄素甲醚干预后细胞活性明显增加（P〈0．05）；大黄素甲醚显著增加上清液中SOD含量（P〈0．05）。缺氧12h后PCR结果分析显示，大黄素甲醚显著降低p38MAPK和Caspase-3mRNA表达量（P〈0．01）。结论大黄素甲醚能增强缺氧所致神经元抗损伤能力，对神经元起保护作用。

Neuroprotective effect of physcion on cultured PC12 cells damage due to anoxia

Objective To explore the effect of of physcion on cultured PC12 cells damage due to anoxia. Methods The PC12 cells were cultured in DMEM. Then these cells were randomly divided into four groups, i.e., control group （normal PC12 cells）, anoxia-treated group （PC12 cells suffered from anoxia damage）, low dose physicon-treated group （PC12 cells were treated with physicon with a concentration of 1 p.g/ml for 12 hours and then suffered from anoxia damage） and high dose physicon-treated group （PC12 cells were treated with physieon with a concentration of 5 p.g/ml for 12 hours and then suffered from anoxia damage）. The activities of PC12 cells, the lever of supernatant superoxide dismutase （SOD）, and the mRNA levels of p38MAPK and caspase-3 were measured before anoxia and 1, 2, 6, 12 and 24 hours after anoxia. Results The activities of PC12 cells and the level of SOD significantly decreased 1 hour after anoxia, the mRNA level of p38MAPK significantly increased 2 hours after anoxia and the mRNA level of caspase-3 significantly increased 6 hours after anoxia in anoxia-treated group compared with control group （P〈0.05）. The activities of PC I2 cells and the level of SOD were significantly higher in physicon-treated groups than those in anoxia-treated group 1 hour after anoxia （P〈0.05）, the mRNA level of p38MAPK was significantly lower 2 hours after anoxia and the mRNA level of caspase-3 was significantly lower 6 hours after anoxia in physicon-treated groups than those in anoxia-treated group （P〈0.05）. Conclusions Physicon can enhance PC 12 cell survival against anoxia damage. The underlying mechanism may be involved in increasing SOD and decreasing p38MAPK and caspase-3.