Abstract: AIM: To investigate the effects of pioglitazone on oxidative stress levels and insulin resistance and initially approach the molecular mechanisms of pioglitazone improving insulin resistance. METHODS: The insulin resistance cell models were induced by TNF-α(4 ng mL) to stimulate human hepatoma carcinoma cell HepG2.The cytotoxicity of HepG2 was observed by MTT.The concentrations of glucose in cell culture fluid of HepG2 were detected using a glucose oxidase assay kit.The levels of intracellular reactive oxygen species were detected by DCFH-DA fluorescent probe and flow cytometry.The expressions of JNK, p-JNK, IRS1 were measured by Western blotting. RESULTS: After HepG2 was stimulated by TNF-α, the glucose uptake was blocked, the glucose concentrations were significantly increased in cell culture fluid, the active oxygen levels were significantly increased in cells, the JNK was activated, the expression of IRS1 was decreased.Pioglitazone could significantly decrease the active oxygen levels, inhibit JNK phosphorylation, promote the expression of IRS1, improve insulin resistance. CONCLUSION: Pioglitazone could improve the insulin resistance condition by degrading oxidative stress levels and inhibiting JNK passway.

Key words: insulin resistance, oxidative stress, TNF-α