中文摘要：

目的：探讨吡格列酮对胰岛素抵抗状态下的氧化应激水平的影响。方法：分别用TNF—α（4ng／mL）和高浓度胰岛素（10^-7mol／L）刺激人肝癌细胞HepG2，建立胰岛素抵抗细胞模型。MTT法观察细胞毒性作用；氧化酶法检测细胞培养液中的葡萄糖浓度；用DCF—DA探针标记，流式细胞仪检测细胞内活性氧的水平；免疫荧光检测NF—κB核转位。结果：TNF—α和高浓度胰岛素刺激HepG2后，导致葡萄糖摄取障碍，细胞培养液上清中葡萄糖浓度较对照组显著升高，同时细胞内活性氧的水平较对照组也显著升高。吡格列酮显著改善胰岛素抵抗状态，同时显著降低细胞内氧化应激的水平。吡格列酮还能逆转TNF—α和高浓度胰岛素引起的NF—κB核转位。结论：吡格列酮能抑制NF—κB核转位，降低氧化应激水平，改善胰岛素抵抗状态。

英文摘要：

AIM：To investigate the effects of pioglitazone on oxidative stress and insulin re sistance. METHODS： The insulin resistance cell model was induced by TNF-α（4 ng/mL）and high dose of insulin（10^-7mol/L） to stimulate human hepatoma carcinoma cell HepG2. The cytotoxic ity of HepG2 was observed by MTT. The concentration of glucose in cell culture fluid of HepG2 was detected using a glucose oxidase assay kit. The level of intracellular reactive oxygen species （ROS） was detected by DCFH-DA fluorescent probe and flow cytometry. The transloeation of NF -κB was observed by immunofluorescence. RESULTS： Compared with control, TNF-α and high dose of insulin treatment significantly increased the level of ROS in HepG2 and the concentration of glucose in the cultrure medium of HepG2. However, pioglitazone treatment could reverse those effects of TNF-α and high dose of insulin. NF-κB translocared to nuclear stimulated by TNF-α and high dose of insulin. Pioglitazone could inhibit the translocation of NF-κB. CONCLUSION： Pioglitazone improve the insulin resistance condition by degrading oxidative stress level and inhibiting the translocation of NF-κB.