Abstract: AIM: To investigate the effects of pioglitazone on oxidative stress and insulin resistance. METHODS: The insulin resistance cell model was induced by TNF-α(4 ng/mL)and high dose of insulin(10^-7 mol/L) to stimulate human hepatoma carcinoma cell HepG2. The cytotoxicity 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 translocation of NF-κB was observed by immunofluorescence. RESULTS: Compared with control, TNF-αand 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 translocated to nuclear stimulated by TNF-αand 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.

Key words: Insulin resistance, Oxidative stress, TNF-α, NF-κB