Mechanism of Apocynin improves insulin resistance induced by TNF-α in HepG2 cells

Abstract

Abstract: AIM: To investigate the effects of Apocynin on oxidative stress and insulin resistance induced by TNF-α. METHODS: Cells were divided into control group,TNF-α(4 ng/mL)treatment group,TNF-α+Apocynin(100 μmol/L)treatment group,Apocynin(100 μmol/L)group. The insulin resistance cell model was induced by TNF-α(4 ng/mL)to stimulate human hepatoma carcinoma cell HepG2. The intracellular glycogen 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 expressions of JNK, p-JNK, IRS1 and p-IRS1 were observed by Western blotting. RESULTS: Compared with the control group, the level of ROS in HepG2 Cells in TNF-α treatment group was significantly increased and the level of intracellular glycogen in cell was decreased, TNF-α activated JNK and inhibited insulin signal pathway,and Apocynin could reverse those effects induced by TNF-α.Apocynin(100 μmol/L)group had no significant effects on ROS,glycogen synthesis and signal pathway. CONCLUSION: Apocynin can decrease the level of ROS in cell and improve insulin resistance condition induced by TNF-α in HepG2 cell.

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

CLC Number:

R965.2

LI Lan-fang, YUO Yu, TANG Guo-tao, YU Cui-yun, CHEN Lin-xi. Mechanism of Apocynin improves insulin resistance induced by TNF-α in HepG2 cells[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2010, 15(10): 1116-1121.

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